An arteriovenous malformation (AVM) is a vascular anomaly in which blood flows directly from arteries to veins without passing through the normal capillary bed. This shortcut forms a tangled cluster of abnormal vessels, commonly called the nidus, that creates a high-flow, high-pressure shunt. AVMs can occur in many parts of the body but are most clinically significant when they involve the central nervous system, especially the cerebral circulation. They are not infectious or cancerous; rather they are structural vascular malformations present from development or early life.

Anatomy and causes

In an AVM the normal microvascular network is replaced by a direct connection that lacks the resistance and filtering role of capillaries. Veins draining an AVM are exposed to arterial pressure, which can lead to dilation, rupture, and bleeding. Most AVMs are described as congenital, arising during vascular development, though the exact genetic and environmental contributors are incompletely understood. Some heritable conditions and specific genetic variants have been associated with vascular malformations, but many cases appear sporadic.

Signs and symptoms

Symptoms reflect the AVM's size and location. When located in the brain, common presentations include persistent or severe headaches and seizures; headaches are a frequent complaint and seizures may be the first recognized sign. AVMs can also present suddenly with bleeding into brain tissue or surrounding spaces, producing a hemorrhagic stroke or other acute neurological decline (intracranial hemorrhage and stroke). Focal neurological deficits, progressive weakness, visual changes, or difficulties with speech and coordination can occur if nearby brain regions are affected.

Diagnosis

Evaluation typically begins with noninvasive imaging such as MRI or CT to localize an abnormality and assess for hemorrhage or mass effect. Definitive vascular anatomy is often defined by angiography; digital subtraction angiography remains the gold standard for visualizing the feeding arteries, nidus, and draining veins. Imaging reports guide risk assessment and treatment planning, and multidisciplinary review by specialists in neurosurgery, interventional neuroradiology, and radiation oncology is common.

Treatment and management

Management is individualized. Options include careful observation for small, low-risk lesions; microsurgical resection for accessible AVMs that can be removed with acceptable risk; endovascular embolization, which uses catheter-delivered agents to reduce flow or occlude feeders; and stereotactic radiosurgery, which targets the nidus with focused radiation to induce gradual closure. Often clinicians combine these approaches to reduce size and risk prior to definitive treatment. Choice of therapy balances the natural risk of hemorrhage against the potential complications of intervention.

Prognosis and important distinctions

The natural history of an AVM varies: some remain stable for years while others cause bleeding or progressive symptoms. Rupture risk depends on factors such as prior hemorrhage, deep venous drainage, and lesion size. AVMs differ from single arteriovenous fistulas and from developmental venous anomalies; accurate diagnosis is important because management strategies differ. Lifelong follow-up with periodic imaging is often recommended after treatment or for monitored lesions.

Resources and further information

  • For general anatomy and vascular terminology see arterial system and venous system references.
  • Guidance on neurological symptoms and stroke is available via specialist sources on intracranial hemorrhage and stroke care.
  • Patient information about common presentations such as headache and seizures can help prompt timely evaluation.
  • For an overview of brain AVM assessment and treatment strategies consult multidisciplinary clinical guidelines or specialist centers (see diagnostic imaging and CNS vascular resources).