Cerebral arteriovenous malformation (AVM) is a congenital vascular anomaly in which arteries drain directly into veins without an intervening capillary bed. The abnormal vascular cluster, called the nidus, consists of feeding arteries and draining veins. It most commonly presents between ages 20-40 with intracranial hemorrhage, seizures, or neurological deficit. The annual hemorrhage risk is 2-4%, and each hemorrhage episode carries 10-15% mortality and 30-50% morbidity. The Spetzler-Martin classification is the gold standard for surgical risk assessment, determined by nidus size, proximity to eloquent areas, and venous drainage pattern. Imaging is critical for diagnosis, classification, and treatment planning; MRI and conventional angiography are the primary modalities.
Age Range
10-40
Peak Age
25
Gender
Equal
Prevalence
Uncommon
Cerebral AVMs arise from a maturational defect in vascular structures developing from the mesenchymal primordium during embryogenesis; the normal capillary bed fails to form, creating low-resistance, high-flow shunts between arteries and veins. In this high-flow state, feeding arteries enlarge, draining veins become arterialized, and turbulent flow occurs within the nidus. This turbulent flow produces the characteristic flow void phenomenon on MR images; rapidly flowing protons cannot generate signal and appear as hypointense tubular structures. The chronic high-flow state leads to feeding artery aneurysm formation, venous stenosis, and peripheral hypoperfusion (steal phenomenon). Hemorrhage typically occurs from fragile vessels within the nidus or rupture of associated aneurysms, and hemoglobin degradation products alter T1/T2 signal characteristics. On SWI sequences, hemosiderin deposition is visualized as magnetic susceptibility artifact because paramagnetic hemosiderin disrupts local magnetic field homogeneity and causes signal loss.
The nidus, feeding arteries, and draining veins appearing together as hypointense serpiginous tubular structures (flow voids) on T2-weighted sequences constitute the signature finding of AVM. This finding distinguishes high-flow vascular malformations from other parenchymal lesions.
Serpiginous hypointense tubular structures (flow voids) are seen on T2-weighted sequences, corresponding to the nidus, feeding arteries, and draining veins. These findings represent the most characteristic MR imaging feature of high-flow vascular malformations. The nidus typically appears as a tangle of intertwined vessels, and surrounding parenchymal T2 signal increase may accompany due to gliosis.
Report Sentence
On T2-weighted sequences, a nidus formation containing serpiginous flow voids is observed in the [location] region, with identifiable feeding arteries and draining veins.
On T1-weighted sequences, the nidus appears isointense or mildly hypointense relative to brain parenchyma; flow voids are identified as hypointense tubular structures. If subacute hemorrhage is present, T1 hyperintensity (methemoglobin) accompanies the finding. Feeding artery enlargement and arterialization of draining veins can be assessed on T1 sequences. On contrast-enhanced T1 images, the nidus shows avid enhancement.
Report Sentence
On T1-weighted sequences, an isointense-to-hypointense nidus formation with flow voids is seen in the [location] region, [with subacute hemorrhage identified/without hemorrhage identified].
On FLAIR sequences, hyperintense signal changes are observed around the nidus due to gliosis. Old hemorrhage areas may appear hypointense due to hemosiderin deposition. FLAIR is superior to T2 for detecting edema and gliosis because it suppresses CSF signal and more clearly reveals perivascular changes. Perilesional edema due to venous congestion may also be seen.
Report Sentence
On FLAIR sequences, hyperintense signal changes consistent with gliosis are seen around the nidus, along with [hemosiderin deposition from prior hemorrhage/edema].
On SWI (Susceptibility Weighted Imaging) sequences, prominent hypointense signal ('blooming' artifact) is observed in old hemorrhage areas due to hemosiderin deposition. This finding reveals occult hemorrhages and detects microbleeds invisible on conventional sequences. In AVMs, multiple hemosiderin foci around the nidus and in parenchyma indicate recurrent subclinical hemorrhage. Deoxyhemoglobin within vessels also appears hypointense on SWI, enhancing vascular detail.
Report Sentence
On SWI sequences, blooming artifact due to hemosiderin deposition is observed around the nidus in the [location] region, along with [multiple hypointense foci related to microbleeds].
On non-contrast CT, AVM appears as a hyperdense hematoma (60-80 HU) during acute hemorrhage. In the absence of hemorrhage, the nidus may be isodense or slightly hyperdense, and calcifications may accompany (in 25-30% of cases). Enlarged feeding arteries and draining veins may be identified as round or tubular hyperdense structures. CT is rapid and effective for acute hemorrhage detection but limited for AVM diagnosis in the absence of bleeding. Subarachnoid or intraventricular hemorrhage extension is also evaluated on CT.
Report Sentence
On non-contrast CT, [a hyperdense hematoma/an isodense to slightly hyperdense nidus formation] is observed in the [location] region, [with accompanying calcifications/without calcifications].
On CT angiography (arterial phase), the AVM nidus shows avid enhancement and early venous filling is observed — direct evidence of arteriovenous shunting. Feeding arteries are seen as enlarged vessels, and multiple arterial feeders may be identified. Draining veins opacify in the arterial phase (normally expected in venous phase). Multiplanar reformats and 3D volume rendering images reveal nidus size, localization, and vascular anatomy in detail.
Report Sentence
On CT angiography, an avidly enhancing nidus formation is observed in the [location] region with early venous filling in the arterial phase, with identifiable [feeding artery/arteries] and [draining vein/veins].
On perfusion MRI (DSC or ASL), markedly increased cerebral blood volume (CBV) and cerebral blood flow (CBF) are observed within the AVM nidus, while perilesional hypoperfusion (steal phenomenon) is detected around the nidus. This indicates that the AVM steals blood from surrounding brain tissue and may contribute to neurological symptoms (seizures, progressive neurological deficit). On ASL (Arterial Spin Labeling) perfusion, arterial transit artifacts may be seen due to shunting.
Report Sentence
On perfusion MR imaging, markedly increased CBV/CBF is observed within the nidus in the [location] region, with perilesional hypoperfusion due to steal phenomenon in the surrounding parenchyma.
On MR angiography (TOF or contrast-enhanced MRA), feeding arteries, nidus, and draining veins are directly visualized. Early venous filling provides hemodynamic evidence of arteriovenous shunting. 4D flow MRA allows quantitative measurement of flow velocities and directions. TOF-MRA produces bright blood images unlike flow voids and is essential for vascular mapping. The venous drainage pattern (superficial vs deep) is a critical parameter for Spetzler-Martin classification.
Report Sentence
On MR angiography, a nidus measuring [size] cm is visualized in the [location] region, with [feeding artery/arteries] and [draining vein(s)], demonstrating early venous filling in the arterial phase.
Criteria
Nidus <3 cm, in non-eloquent area, superficial venous drainage only. Total score 1-2 points. Low surgical risk, high complete resection success rate (95%+).
Distinct Features
Small compact nidus, limited number of feeding arteries and draining veins, minimal effect on surrounding parenchyma, perilesional edema/gliosis usually limited. Appears as a localized cluster of flow voids on imaging.
Criteria
Total score 3 points (various combinations: medium size+eloquent, large size+non-eloquent, small+eloquent+deep drainage, etc.). Variable surgical risk, requires detailed evaluation.
Distinct Features
Nidus size, localization, and drainage pattern are variable. Subgroup analysis is critical: Grade III-A (small nidus+eloquent+deep drainage) vs Grade III-B (large nidus+non-eloquent+superficial drainage) have different prognoses. Imaging requires both structural and functional assessment.
Criteria
Total score 4-5 points. Large nidus (>6 cm), in eloquent area, with deep venous drainage. High surgical risk, complete resection difficult with high morbidity rate. Conservative management or multimodal approach (embolization+radiosurgery) is usually preferred.
Distinct Features
Large, diffuse nidus, multiple feeding arteries and draining veins, prominent perilesional effect (gliosis, edema, atrophy), frequently associated aneurysms, prominent steal phenomenon. Imaging shows complex vascular structures occupying a large area with prominent changes in surrounding parenchyma.
Criteria
AVM presenting with acute intracranial hemorrhage. Intraparenchymal, subarachnoid, or intraventricular hemorrhage may accompany. The nidus may show partial thrombosis after hemorrhage. Requires urgent neurosurgical evaluation.
Distinct Features
Acute hyperdense hematoma on CT, stage-dependent signal changes on MRI (hyperacute→acute→subacute→chronic), prominent hemosiderin deposition on SWI, active extravasation or pseudoaneurysm on DSA. Hemorrhage may mask the nidus, and the nidus should be reassessed on follow-up imaging.
Distinguishing Feature
Cavernous malformation (cavernoma) is a low-flow vascular lesion and does not show flow voids on T2. It has a characteristic 'popcorn' appearance: mixed signal intensity center (blood products at various stages) with a complete surrounding hemosiderin rim. Unlike AVM, it is angiographically occult (angiographically negative) and does not demonstrate feeding arteries or draining veins.
Distinguishing Feature
Glioblastoma is an intra-axial mass with avid ring or irregular enhancement. Central necrosis, perilesional edema, and mass effect are prominent. Unlike AVM, it does not show flow voids (weak vascular structures), perfusion shows increased CBV but no early venous filling. It may show diffusion restriction on DWI (cellular tumors), whereas AVM does not demonstrate parenchymal diffusion restriction.
Distinguishing Feature
Hemangioblastoma typically locates in the posterior fossa (cerebellar) and shows a cystic component + avidly enhancing mural nodule pattern. Flow voids may be seen due to increased vascularity, but these are more limited and organized compared to AVM, lacking the distinct nidus-feeding artery-draining vein triad. It is associated with Von Hippel-Lindau syndrome. Perfusion shows increased CBV but no early venous filling.
Distinguishing Feature
Hypervascular metastases (renal, thyroid, melanoma) show avid enhancement and rarely may contain perilesional flow voids, but lack AVM's characteristic nidus+feeding artery+draining vein triad. Metastases are typically multiple, located at the gray-white matter junction, show prominent perilesional edema, and have known primary malignancy history. MR spectroscopy shows elevated choline/creatine ratio (cellular proliferation) while AVM shows no spectroscopic abnormality.
Distinguishing Feature
Primary CNS lymphoma is a homogeneously avidly enhancing mass with periventricular or deep gray nuclei localization. It shows prominent diffusion restriction on DWI (high cellularity). Unlike AVM, there are no flow voids; perfusion shows CBV increase but milder than AVM and no early venous filling. It is common in immunosuppressed patients (HIV, transplant) and dramatic regression with steroid therapy (ghost tumor) aids diagnosis.
Urgency
highManagement
Multidisipliner — norocerrahi/nororadyoloji/radyocerrahi ekibi. Tedavi secenekleri: mikrocerrahi rezeksiyon (dusuk dereceli), endovaskuler embolizasyon (preoperatif veya definitif), stereotaktik radyocerrahi (kucuk, derin yerlesimli), kombinasyon tedavisi veya konservatif takip (yuksek dereceli).Biopsy
Not NeededFollow-up
Tedavi sonrasi MR anjiyografi + konvansiyonel anjiyografi ile tam obliterasyon dogrulama. Radyocerrahi sonrasi 2-3 yil takip. Yillik MR takip onerili.Cerebral AVM is a congenital vascular anomaly carrying an annual hemorrhage risk of 2-4%. Each hemorrhage episode is associated with 10-15% mortality and 30-50% morbidity. The Spetzler-Martin classification is essential for treatment planning: Grade I-II are surgical candidates, Grade IV-V usually require conservative or multimodal approach. Imaging is mandatory for diagnosis, classification, and treatment planning; MRI+MRA is the primary modality, conventional angiography (DSA) is the gold standard. In unruptured AVMs, treatment decisions are based on individual risk-benefit analysis in light of the ARUBA trial results.
Cerebral AVMs carry 2-4% annual hemorrhage risk. Treatment options include microsurgical resection, stereotactic radiosurgery (Gamma Knife), endovascular embolization, or combination thereof. Spetzler-Martin Grade 1-2 lesions are best surgical candidates. Prior hemorrhage increases rebleeding risk.