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Arteriovenous malformations (AVMs) are congenital vascular lesions. They are characterized by an abnormal connection between arteries and veins that lack an intervening capillary bed, which results in direct arteriovenous shunting. AVMs are the most common of the four types of vascular malformations in the central nervous system, the other three being developmental venous anomalies (DVA), cavernous malformations (CM), and capillary telangiectasias.1-3


In general, the etiology of AVMs is complicated and not well understood. It was originally thought that AVMs arise due to failure around the third week of embryogenesis in the differentiation of vascular channels into mature arteries, capillaries, and veins. However, as AVMs are rarely detected in utero or found in infants, some researchers suggest that AVMs develop later in life.4 Studies have also shown that AVMs may arise postnatally.4,5 Most theories suggest either persistence of a primitive arteriovenous connection or the development of such after the initial closure of the primitive connection.1,2 Other theories suggest that AVMs develop due to deranged vessel growth, remodeling dysfunction at the capillary-venous junction, or fistulization of cerebral venous angiomas.4 AVMs are thought to have multifactorial causes, including genetic manipulation and angiogenic stimulation.5,6 AVMs follow an autosomal dominant inheritance pattern in a heterozygous matter. The homozygous forms are lethal. Multiple candidate genes and pathways have been identified for the genetic basis of intracranial AVMs, such as endoglin (ENG) on chromosome 9q and activin-receptor-like kinase (ALK1) on chromosome 12q. In addition, genetic anomalies have been found to increase the risk of AVM rupture. In particular, matrix metalloproteinase-9 (MMP-9) alterations can compromise vascular stability and lead to irregular angiogenesis.4,7


The overall incidence of AVMs is difficult to estimate as they are not commonly found unless complications arise. It is a rare, usually sporadic disease and has no sex predilection. Its current incidence and prevalence are unknown.8 Cerebral AVMs are a common cause of intracranial hemorrhage in children (excluding hemorrhage in prematurity and early infancy), representing about 30-50% of pediatric hemorrhagic strokes.1,2,9 Spinal cord AVMs comprise 20-30% of all spinal vascular malformations and are the most common cause of nontraumatic intraspinal bleeding or hematomyelia.10

In general, they occur sporadically with rare familial incidence, and a few reports mention an association with other abnormalities like hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu disease), Wyburn–Mason syndrome, von Hippel–Lindau disease, and Sturge–Weber syndrome.1,3,11 Hereditary hemorrhagic telangiectasia, an autosomal-dominant disease, is the most common genetic cause of cerebral AVM and carries a 10–25% lifetime risk of developing a cerebral AVM.12 Assuming a constant annual risk of hemorrhage of 2–4%, the lifetime risk of hemorrhage in patients with AVM can be estimated using the following formula: Lifetime risk = 1 − (Risk of no hemorrhage) Years of remaining life.4

Patho-anatomy and physiology

There is a structural defect in the formation of the arteriolar capillary network that is normally present between arteries and veins. Due to the absence of capillary communication, shunting elevates intraluminal venous pressure and produces ectasia and muscularization that form hybrid vessels and a vascular network called a nidus (nidal-type) or mainly a direct connection between the artery and the vein (fistulous-type). Over time, the lesion enlarges due to pressure differentials. Hemorrhage is thought to be due to the non-static nature of the AVMs and the rapid expansion that can occur during times of growth, possibly related to angiogenic/vascular growth factors.1,9 Hemorrhage is often associated with increased pressure in feeding arteries and draining veins (i.e., outflow restriction).4 Hemorrhage occurs in 0.5% of cases of cranial AVMs and is more common with the fistulous type.8

In children, there is a higher incidence of AVMs in the posterior fossa, basal ganglia, and thalamus, which are more prone to bleeding and may result in catastrophic outcomes.1 In the spinal cord, the nidus-type AVM has been associated with an increased risk of bleeding, and the fistulous-type typically presents as progressive myelopathy due to its mass effect.10 Spinal AVMs are also associated with asymmetric growth in children.8

Disease progression

The natural history of AVMs in the pediatric population is not well understood. It is the most common cause of spontaneous intracranial hemorrhage in children, with 80–85% of pediatric patients suffering a hemorrhagic event as the initial presenting symptom. Seizures are a common presenting symptom of AVMs in the frontal lobe.13 Overall, the presentation of symptoms depends on the location and extent of the brain or spinal cord involved and whether it is caused by hemorrhage or ischemia as a result of compression from venous congestion. Risk factors for AVM hemorrhage include a previous history of hemorrhage (within 5 years), a deep-seated or infratentorial location, an exclusive deep venous drainage, nidal-type, association with an aneurysm, and diffuse morphology.1,2,14 Large, deep lesions have significant morbidity and are associated with high rates of rupture and neurologic deficits.15

Secondary conditions and complications

AVM is the most unpredictable vascular malformation. It usually remains quiescent in childhood but tends to enlarge with time and cause local destruction.8 Cerebral AVMs may present with intracranial hemorrhage, seizures, headache, and focal neurologic deficits that may result in long-term disability. Neurologic symptoms are dependent on location within the brain or spinal cord, presenting either as a stroke or progressive myelopathy, respectively.1,16

Acute hemorrhagic events in children have been associated with up to a 25% mortality rate.1 A hemorrhagic presentation is a significant independent predictor of future hemorrhage. The annual risk of rebleeding in children is 2–4% but may be up to 65% when projected over the child’s lifespan.1 In the spinal cord, lesions with persistent perimedullary veins and those located in the cervical and upper thoracic level appear to have a higher risk of rehemorrhage.17

Essentials of Assessment


A detailed history that focuses on components similar to other acquired brain or spinal cord injuries including symptom timing and onset of headache, seizures, weakness, visual or swallowing abnormalities, progressive limb weakness, as well as bladder and bowel symptoms is important. Characteristics of headache and back pain may be non-specific, although some may report persistence in a localized area. AVMs may also cause subtle learning and behavioral disorders in some children long before more obvious symptoms become evident.18,19


A comprehensive physical examination with focus on the neurological exam as one would do for a patient with a stroke or myelopathy is warranted, keeping an eye out for asymmetries, signs/symptoms of intracranial pressure or evidence of spinal cord compromise. Neurologic findings can include limb weakness/paralysis, ataxia, apraxia, sensory, visual, and cranial nerve abnormalities, dizziness, aphasias, mental status and cognitive impairments, hallucinations, dementia, gait imbalance and bladder and bowel dysfunction. A particularly severe type of AVM causes symptom to appear soon after birth as a major blood vessel is involved This is called the vein of Galen defect. It is associated with hydrocephalus and presents with seizures, failure to thrive and congestive heart failure.20 Presence of vascular skin lesions may be associated with some hereditary/genetic abnormalities like Osler-Weber-Rendu disease and Sturge-Weber Syndrome, which may warrant further diagnostic work-up and genetic testing.3   

Clinical functional assessment

Depending on the area of involvement and symptom presentation, one may utilize the clinical functional assessment tools such as the Glasgow Coma scale, Pediatric National Institutes of Health Stroke Scale (NIHSS) , modified Rankin scale, American Spinal Injury Association (ASIA) Impairment Scale and Functional Independence Measure for children (WeeFIM). Cognitive, speech and neuropsychological evaluation may also be needed.

Lab studies

There is no specific laboratory study for AVM’s; however, based on its presentation and secondary medical complications, one may monitor CBC, metabolic panel, renal panel and coagulation studies. Several genetic polymorphisms have been identified that exacerbate lesion progression and increase the risk of AVM rupture owing to increased expression of IL-6, IL-1β, IL-1α, TNF-α, and IL-8. However, these inflammatory markers are more useful to plan therapeutic strategies.21


AVMs are usually diagnosed through a combination of magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), computed tomography (CT) and digital subtraction angiography (DSA). These imaging studies may need to be repeated to analyze a change in the size of the AVM, presence of hemorrhage, any calcification or the appearance of new lesions.12,19 MRI with and without contrast, with MRA of the brain and/or spine helps to rule out other hemorrhagic lesions such as tumors and cavernous malformations, and can better delineate the vascular anatomy of the lesion. These imaging studies may all be used in combination to compile a clearer picture of the AVM. DSA remains the gold standard, as it provides the greatest sensitivity and detail of all the imaging types.12

Supplemental assessment tools

Imaging studies of other areas of the body such as the lung, liver, spleen and the gastrointestinal tract may be done to rule out other possible associated vascular anomalies. Cardiac work-up may be needed in cases of suspected cardiovascular compromise due to the shunting phenomenon in certain types of vascular malformations. These are more commonly seen in developmental vein anomalies and less commonly with AVM’s.3,20

Early prediction of outcomes

There have been few studies of long-term clinical outcomes of brain AVMs in pediatric patients, and previously published studies have used conventional metrics that have been validated in the adult population, such as the modified Rankin Scale. Although these metrics can serve as reasonable surrogates, an accurate understanding of overall health-related quality of life is contingent on utilizing validated toolsets, such as the pediatric quality of life inventory PedsQL.22

AVMs are often an incidental finding versus a catastrophic presentation due to rupture/hemorrhage, making prediction of outcomes difficult. Once neurological deficit occurs, focus is on prevention of symptom worsening with secondary measures. Once rupture or hemorrhage occurs, there is an increased risk of recurrence, especially in the first year. Nidus-type spinal cord AVMs had lower complete obliteration rates that may cause delayed rebleeding and clinical progression from hemorrhage to myelopathy and long-term deterioration.16 Close monitoring of these lesions are necessary. Incidentally found AVMs have several factors that may be used to estimate the risk of hemorrhagic presentation. AVMs with associated aneurysm, a single draining vein, a single feeder, deep venous drainage, infratentorial location, deep location, diffuse morphology, and a high Spetzler-Martin (SM) grade have a higher risk of hemorrhage.12,23The Spetzler-Martin Grade (SMG) scale is commonly used as a grading scale to predict the risk of surgical morbidity and mortality with brain AVMs. It is a composite score of nidus size, eloquence of adjacent brain and presence of deep venous drainage. Higher scores suggest increased surgical morbidity and mortality risk.24


Depending on the neurologic sequela and resultant disability, ongoing physical, occupational and speech therapy, child life services and social services may be warranted. Home and environmental modifications, along with adaptive equipment and mobility/gait aids may be needed to accommodate for resultant persistent functional impairments.


Acute neurologic sequala with resultant functional impairment from an acquired brain or spinal cord injury requires good family and social support. As the child transitions back into the home, school and community, proper accommodations and assistance may be required for mobility and activities of daily living. Support, counseling, education, and developmental guidance is needed for family and other caregivers. Resources for opportunities to be creative and social for children of all ages, including infants and teens, is beneficial.


There is often a delay in diagnosis due to the low overall incidence, thus heightened clinical suspicion is necessary for prompt diagnosis. In the initial phase, when emergent symptoms are being controlled and addressed, there may be a delay in definitive treatment of the AVM. This may pose as a stressful time for patients and families with concerns about the risk of recurrence of emergent symptoms.

Rehabilitation Management and Treatments

Current treatment guidelines

Treatment may be conservative or interventional depending on lesion features, clinical presentation and patient specific factors.25 Treatment options include endovascular embolization via catheter delivery of liquid embolics or coils, microsurgical resection, and stereotactic radiosurgery (e.g., Gamma knife). Embolization alone rarely represents a curative treatment. However, a reduction in the size of the nidus or AVM flow may enable the performance of stereotactic radiosurgery or facilitate surgical removal. The risk of all treatment modalities should be weighed against the natural history risks of AVMs. The Spetzler-Martin (SM) grading scale is utilized as a decision tool to estimate the risk of surgical resection by evaluating the AVM size, pattern of venous drainage and eloquence of brain location, with higher grades of 4 and 5 being associated with greater surgical morbidity and mortality.1,16,26  Generally, AVMs with high grades are managed with conservative management due to rupture risk and worse prognosis with operative treatment including partial resection.15,25,27 Further, there is evidence that medical management alone of unruptured AVMs of the brain is superior to interventional therapy or medical plus interventional therapy at 5 year follow up.27

At different disease stages

Acute: Observation, medical management and emergent surgical intervention may be warranted based on AVM characteristics and clinical presentation. With acute hemorrhagic presentation, prompt life saving measures to prevent further neurologic compromise are essential. Definitive treatment may be delayed to allow for characterization, healing, or adjuvant therapy as part of a staged treatment plan due to the size, location and complexity of the lesion.16 However, despite variances in clinical courses, treatment outcomes, and complications, pediatric patients with AVMs who underwent acute inpatient rehabilitation saw improvement in their WeeFIM scores upon discharge.28

Subacute: Depending on the location and type of vascular malformation, subsequent monitoring of the lesion with symptom presentation and imaging studies is done. This will guide further need for surgical intervention with a goal of lesion obliteration and prevention of re-bleeding and further neurologic sequela. In some asymptomatic AVMs that are incidentally found, clinical observation with monitoring is appropriate.16

Chronic/stable: Long term follow-up is necessary due to risk of recurrence and re-rupture. There are currently no established guidelines for length of monitoring. New or evolving symptoms warrant additional imaging/workup to ensure stability of the vascular lesion. Neurologic deficits may improve or persist indefinitely.16 Rehabilitation strategies apply as with any other cause of acquired brain or spinal cord injury. (Please see rehabilitation care for pediatric stroke and spinal cord injury).

Coordination of care

To date, no definitive guidelines exist for the management of brain and spinal AVMs. Multispecialty interdisciplinary care is vital given the complex nature and course of AVMs with the risks of intervention balanced against the natural course of each individualized treatment strategy.29 This pertains to both medical/surgical management of the vascular lesion as well as in the rehabilitation management of acquired brain and spinal cord injury.

Patient and family education

Patient and family education as to the diagnosis and possible treatment options, with a good understanding of its risk and benefits, as well as the need for subsequent follow-up and rehabilitation cannot be over-emphasized. With the high rate of persistent neurological deficits, it is important to be able to counsel families on the likelihood of long-term deficits following AVM surgeries. These neurological deficits can be predicted using preoperative deficits, lesions of the eloquent cortex, and AVMs > 3 cm.30

Measurement of treatment outcomes

Treatment must prevent recurrence that can worsen clinical status. Outcome measures are mainly based on prevention of rebleeding and subsequent further neurologic deficits. Rates of recurrence for pediatric brain AVMs are relatively high as compared to adults, up to 13.5% even after complete obliteration.31 This underscores the importance of long term follow up with serial clinical assessments and imaging studies including MRI and DSA to guide treatment outcomes. DSAs are obtained at predefined intervals (i.e., after treatment, at 6 months, and at 5 years) for confirmation of cure.32 Functional outcome measures such as the WeeFIM may be used for those who develop persistent neurological deficits with resultant functional impairments.

Translation into practice

AVM ruptures in children can cause debilitating neurological deficits such as dystonia, hemiparesis, spasticity, hydrocephalus, epilepsy, and ataxia. Although there is little in literature detailing rehabilitation outcomes for children with AVM ruptures, it is clear with the current literature that rehabilitation is vital during the recovery process.28

Cutting Edge and Emerging Concepts

The National Institute of Neurological Disorders and Stroke (division of the NIH) has active and ongoing research in the field of AVMs and other vascular malformations. Currently, studies are underway to better predict natural history and subsequent risk of rupture. This includes utilization of beta-blockers for treatment of AVMs as well as research into specific biomarkers that can aid in risk assessment and treatment selection. In the past decade, multimodality planning with a multidisciplinary team approach has been emphasized to customize the best treatment approach for each individual. The use of noninvasive radiosurgery seems to have surpassed microsurgery and has been shown to have reasonable obliteration rates.16 A recent longitudinal study following patients over a five-year period following stereotactic radiosurgery had a obliteration rate of 60.6% and a hemorrhage rate of 0%, suggesting it is gradually effective and safe.25Each case should still be treated on an individual basis, although radiosurgery is indicated in spinal cord AVMs with higher risk of hemorrhage.12 Current studies show that the new Supplemented Spetzler-Martin (Supp-SM) grading system has superior predictive ability on surgical outcomes when compared to the Spetzler-Martin grading scale (SMS). In addition to the original SMS factors, the Supplemented Spetzler-Martin adds history of hemorrhage, age, and nidus type. This scale has also proved to be helpful in decision making on Grade III lesions, which still cause clinical controversy.33 Additionally, the use of arterial spin labeling MRI is showing some potential as a noninvasive diagnostic and follow-up study of pediatric AVMs with emerging evidence as a useful radiation- and injection-free noninvasive biomarker to objectively delineate treatment effect and aid in treatment planning.26

Visual impairments in those with brain injuries, such as those from AVM ruptures, are hard to access with current methods due to co-occurrence with cognitive and communication disabilities. A recent study developed a system to grade vision health through eye movements and gaze-based tacking behaviors. This system can be used for both communicative and non-communicative pediatric patients. Quantitative assessments such as these for this patient population can aid as objective diagnostic tools and as therapy tools.34

Gaps in Evidence-Based Knowledge

Neurovascular lesions remain a considerable cause of morbidity and mortality. The mechanism of lower reported recurrence rates in adults than children remains unclear, though if better understood could guide risk stratification and prevention.31 While noninvasive brain imaging has led to increase in identification of these lesions, significant gaps remain in management decisions given its poorly defined natural history and relatively low incidence, making it difficult to do prospective studies to attain more rigorous data.26 Some of these gaps include the need for multicenter studies to design predictive models in patient selection for multimodal pediatric care so additive morbidity can be avoided.35 There also exists significant gaps on long-term follow up of different treatment modalities comparing the results for unruptured and ruptured brain AVMs.36 Research is still lacking in measurement of risk in regard rupture, re-rupture, treatment, and medical management.37


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  36. Pezeshkpour P, Dmytriw AA, Phan K, et al. Treatment Strategies and Related Outcomes for Brain Arteriovenous Malformations in Children: A Systematic Review and Meta-Analysis. AJR Am J Roentgenol. 2020;215(2):472-487.
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Original Version of the Topic

Rochelle T. Dy, MD, Catherine Schuster, MD. Vascular malformations of the brain and spine in children. 9/14/2015

Previous Revision(s) of the Topic

Catherine Schuster, MD, Michael Stoltz, BS, David Means, BS, Rochelle T. Dy, MD. Vascular malformations of the brain and spine in children. 10/8/2019

Author Disclosure

Saylee Dhamdhere, MD
Nothing to Disclose

Kayla Williams, MD
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Nikhil Gopal, MBBS
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Warona Mathuba, BS
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Rajashree Srinivasan, MD, MBBS
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