Cerebral arteriovenous malformations (bAVMs) are relatively uncommon errors in the development of the vasculature that create complex conglomerates of abnormal arteries and veins linked by one or more fistulae without an intervening capillary bed. They account for the majority of childhood hemorrhagic strokes, and represent the most common cause of nontraumatic intracranial hemorrhage (ICH) in young adults showing a very low prevalence. Current treatment options for bAVM focus on removal or obliteration of the lesion in an attempt to protect against future ICH risk. Due to the malformation, a complex sequence of pathological processes includes extracellular matrix remodeling, and thus disruption of the Blood Brain Barrier (BBB), inflammation and loss of patient functionality. However, to date the pathophysiology of AVMs has been scarcely investigated from both a clinical and preclinical point of view. For this reason, this talk will show latest results from the lab on the pathophysiology of experimental bAVMs through the evaluation of neurovascular alterations, inflammation and BBB disruption (BBBd) using a combination of neuroimaging methods such as positron emission tomography (PET) and magnetic resonance imaging (MRI).