• Michael Söderman, Tommy Andersson, Bengt Karlsson, M Christopher Wallace, and Göran Edner.
• Department of Neuroradiology, Karolinska Hospital, S-17176, Stockholm, Sweden. michael.soderman@ks.se
• Eur J Radiol. 2003 Jun 1; 46 (3): 195-205.

AbstractArteriovenous malformations (AVMs) of the brain, which are probably genetically determined, are errors in the development of the vasculature that, together with the effects of blood flow, may lead to a focal arteriovenous shunt. Clinically, the adult patient may present with acute or chronic neurological symptoms-fixed or unstable-such as deficits, seizures or headache. Sometimes the lesion is an incidental finding. In about half of the patients, the revealing event is an intracranial haemorrhage. The prevalence of AVM in the western world is probably <0.01% and the detection rate is about one per 100,000 person-years. Most AVMs are revealed in patients 20-40 years of age. Therefore, the risk of developing neurological symptoms from an AVM, usually because of haemorrhage, increases with patient age. In the young adult population, AVMs are significant risk factors for hemorrhagic stroke. This risk increases with AVM volume and is higher in centrally located AVMs. Almost all patients with AVM are subjected to treatment, either by surgery, radiosurgery or embolisation, with the functional aim of reducing the risk of haemorrhage or to alleviate neurological symptoms with an acceptable treatment risk. Few neurocentres have physicians highly skilled in all treatment modalities. Therefore, the prescribed treatment may not be defined from an objective assessment of what is optimal for each individual patient, but rather from local expertise. In this context, more and better data about the natural history and the outcome of different treatments, as well as predictive models, would be valuable to help to optimise the management. Management strategies obviously differ according to local preferences, but results presented in the literature suggest the following strategy: (I) cortically located AVMs with a nidus volume <10 ml could be operated, with or without presurgical embolisation, unless there is a single feeder that can easily be catheterised and embolised for obliteration or other obvious target for embolisation, such as pseudoaneurysms or large fistulae; (II) centrally located AVMs with a nidus volume <10 ml should be treated by radiosurgery, unless suitable for embolisation as indicated above; (III) patients harbouring AVMs with a nidus volume >10 ml could benefit from targeted partial embolisation followed by radiosurgery or surgery, depending on the angioarchitecture; and (IV) AVMs >20 ml nidus volume usually have a high treatment risk with any treatment modality and are not obvious targets for treatment at all.

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