**1. Introduction**

AVM is a tangled web of blood vessels, in which arteries directly transition into veins without intermediate microcirculation elements that provide perfusion to surrounding tissue. The AVM blood vessels are called a nidus and have little resistance to flow compared with a normal capillary bed. Such structure manifests violent flows which result in increased hemorrhage risks. Due to growing use of advanced imaging modalities, there has been increased incidental detection of cerebral AVMs. When detected, there is impending need for treatment since stroke chance for an unruptured and untreated AVM is ~20–40% per decade [1]. About 38–71% of patients presenting brain AVM suffer intracranial hemorrhage [2]. Given these statistics, interventional treatment appears vital. Currently, three prevalent modalities exist: endovascular embolization, stereotactic radiosurgery (SRS), and surgical resection. Each modality conveys a wide risk array (safety/efficacy). Thus, many AVMs ultimately remain untreated (see further data below). Unfortunately, these are typically the larger AVMs that could better benefit from intervention (~76% of AVMs having a nidus <30 mm are treated; compared with ~57% of those having a nidus of 30–59 mm and only ~14% of those having a nidus >60 mm) [3]. Moreover, embolization typically necessitates a series of interventional procedures/ sessions (up to 11, on average 2.6) [4]. Each procedure involves patient hospitalization, advanced imaging, general anesthesia, and a high-risk operation but, most importantly, exhibits a 3.2% chance of significant complications [4]. Finally, due to a low obliteration likelihood (11–40%), embolization is not recommended as a single-modality therapy and is usually combined with radiosurgery. Radiosurgery (if successful) takes 1–3 years to achieve obliteration. Thus, patients remain at hemorrhage risk for a lengthy treatment period [5]. To conclude, many patients with cerebral AVM benefit less from current prevalent treatment modalities that carry high risks, costs, and intensive procedures and, even if eventually effective, take years to complete. In 2014, the largest randomized trial on AVMs (ARUBA trial) found that patients treated using the prevalent interventional strategies were three times more likely to suffer a stroke or die compared with those treated only for blood pressure reduction [6]. ARUBA elicited a plethora of reactions. Some were relatively supportive, but many more criticized the study methods and outcomes. Eventually, the controversy led the European societies dealing with AVM to organize a consensus conference. A clear accord emerges. There is, indeed, a lacuna or at least weakness of interventional modalities when addressing high SM grade AVMs. The lack of clear treatment choice for a pathology with a point prevalence of ~18/100,000 in adults responsible for 4% of all primary intracerebral hemorrhages is the motivation for this review [7].

#### **1.1 Definitions and angioarchitecture**

AVM features a vascular region lacking transition hierarchy, where arteries change directly into veins (**Figure 1**) [13]. AVM physical appearance is a welldefined enclosed volume of entangled blood vessels mostly known as a "nidus." Arteries entering the nidus are termed "feeding arteries" and veins leaving it are termed "draining veins" (**Figure 2**) [9].

AVMs may appear in virtually every vascular body region. Clinically, significant AVMs are mainly classified as CNS (cerebral), pulmonary, abdominal, renal,

**Figure 1.** *AVM angioarchitecture [9].*

*Advocating Intraluminal Radiation Therapy in Cerebral Arteriovenous Malformation Treatment DOI: http://dx.doi.org/10.5772/intechopen.89662*

hepatic, and peripheral [8–16]. This chapter focuses on cerebral AVMs due to the high risks and challenging treatment involved with this class. Nidus sizes vary in diameter between 1 and 10 cm. AVMs <3 cm are classified as "small." AVMs between 3 and 6 cm are classified as "medium." AVMs >6 cm are considered as "large" [8]. The majority of AVMs are medium sized (~55%), followed by small (~38%) and then large (~7%) [17, 18]. The nidus structure does not typically obstruct blood flow; in fact, the opposite is true (see below). Thus, the organ function is usually preserved. However, in rare cases (especially large AVMs), the nidus is orientated or structured in a way that impedes perfusion (steal phenomena) [9]. Here, clinical features of ischemia or lack of brain function may be present [17].
