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Arteriovenous Malformations Clinical Presentation

  • Author: Souvik Sen, MD, MPH, MS, FAHA; Chief Editor: Helmi L Lutsep, MD  more...
Updated: Mar 27, 2014


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  • AVMs tend to be clinically silent until the presenting event occurs. Therefore, the diagnosis usually is made at the time of the first seizure or hemorrhage.
  • A history of minor learning disability is present in as many as two thirds of patients; such dysfunction is rarely apparent in adult life.
  • A history of headaches is present in as many as half of patients with cerebral AVM. The headaches subsequently may take the form of classic migraine or more generalized headache.
  • If seizures have occurred, a careful seizure history should be obtained. Seizures are simple, partial, or secondarily generalized.
  • The effectiveness of anticonvulsant therapy should be observed carefully and monitored before and during treatment.


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  • Focal neurologic findings are rare in the absence of seizure or hemorrhage in patients with cerebral AVMs. They are more common in brainstem and deeply located AVMs. They are associated with patient’s age and are more common among women.
  • Detailed neuropsychological testing may disclose subtle right or left hemisphere dysfunction.
  • If parenchymal hemorrhage is present, the physical findings are indistinguishable from those due to intracranial hemorrhage of other causes.
  • Intraventricular hemorrhage generally produces a less severe neurological deficit than hemorrhage into other areas of the brain.
  • In the rare patients in whom focal neurological deficits are present, the deficit may reflect the location of the AVM.


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  • No genetic, demographic, or environmental risk factors for cerebral AVM have been identified clearly.
  • Families with cerebral AVMs are rare, and such pedigrees have been too small to enable linkage studies. From the few family cases reported, the inheritance appears to be autosomal dominant.
  • In a small minority of cases, cerebral AVMs are associated with other inherited disorders, such as the Osler-Weber-Rendu syndrome (ie, hereditary hemorrhagic telangiectasia), Sturge-Weber disease, neurofibromatosis, and von Hippel-Lindau syndrome.
Contributor Information and Disclosures

Souvik Sen, MD, MPH, MS, FAHA Professor and Chair, Department of Neurology, University of South Carolina School of Medicine

Souvik Sen, MD, MPH, MS, FAHA is a member of the following medical societies: American Academy of Neurology, Association for Patient-Oriented Research, American Heart Association

Disclosure: Nothing to disclose.


James Selph, MD Assistant Professor of Neurology, University of South Carolina School of Medicine; Director of Neurophysiology Lab and Services, Palmetto Richland Hospital

James Selph, MD is a member of the following medical societies: American Association of Neuromuscular and Electrodiagnostic Medicine, American Epilepsy Society

Disclosure: Nothing to disclose.

Sharon W Webb, MD Assistant Professor of Clinical Neurosurgery, University of South Carolina School of Medicine

Sharon W Webb, MD is a member of the following medical societies: American Association of Neurological Surgeons, Congress of Neurological Surgeons, Neurocritical Care Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Additional Contributors

Edward L Hogan, MD Professor, Department of Neurology, Medical College of Georgia; Emeritus Professor and Chair, Department of Neurology, Medical University of South Carolina

Edward L Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, Society for Neuroscience, American Society for Biochemistry and Molecular Biology, American Academy of Neurology, American Neurological Association, Phi Beta Kappa, Sigma Xi, Southern Clinical Neurological Society

Disclosure: Nothing to disclose.

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Axial T2 MRI showing an arteriovenous malformation with hemorrhage, in the territory of the left posterior cerebral artery.
T1 axial MRI showing a small subcortical arteriovenous malformation in the right frontal lobe.
T2 coronal MRI showing an arteriovenous malformation in the left medial temporal lobe.
Magnetic resonance angiography showing a left medial temporal arteriovenous malformation.
Angiogram (anteroposterior view) showing an arteriovenous malformation in the deep left middle cerebral artery territory measuring approximately 3 cm in diameter, with a deep draining vein (arrow).
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