A 75-year-old man presented with episodic involuntary chewing movements and restlessness, each lasting between one and two minutes and followed by complete amnesia. Neurological examination was unremarkable, revealing no significant abnormalities, and electoencephalogram (EEG) showed no epileptic activity. Brain MRI was performed, revealing chronic ischemic microangiopathy and lobar microhemorrhages. Additionally, susceptibility-weighted imaging (SWI) demonstrated ectasia, redundancy, and tortuosity of multiple venous structures in the posterior fossa, with marked hyperintensity in right paravermian veins (Figure 1). These findings were highly suggestive of an arteriovenous shunt. Digital subtraction angiography confirmed a dural arteriovenous fistula (dAVF) fed by branches of both occipital arteries (Figure 2).

Figure 1.

Susceptibility-weighted imaging on axial (A), coronal (B), and sagittal (C) reformats shows hyperintensity in vermian veins (arrow), suggesting an arteriovenous shunt.

Figure 1 Long description

Panel A: An axial susceptibility-weighted imaging (SWI) scan of the brain showing hyperintensity in the vermian veins, indicated by an arrow. Panel B: A coronal SWI scan of the brain with an arrow pointing to hyperintensity in the vermian veins. Panel C: A sagittal SWI scan of the brain with an arrow marking hyperintensity in the vermian veins.

Figure 2.

Angiography images (A, B, C) and sagittal 3D reformatted digital subtraction angiography image (maximum intensity projection 12 mm) (D) depict a dural arteriovenous fistula, supplied by occipital artery branches.

SWI is a non-contrast MRI sequence that has emerged as a valuable tool for detecting vascular anomalies such as dAVFs. It is more sensitive than conventional gradient-echo imaging in visualizing venous structures, allowing detailed assessment of venous caliber, drainage patterns, and oxygenation status.^{Reference Haacke, Mittal, Wu, Neelavalli and Cheng1} In cases of dAVF, SWI can reveal abnormal venous hyperintensity (signal equal to or greater than proximal intracranial arteries), which contrasts with the typical hypointense signal of normal veins due to deoxyhemoglobin. This hyperintensity is attributed to a combination of intrinsic time-of-flight effects, caused by high arterial flow velocity, and the lack of paramagnetic phase effects, due to the predominance of diamagnetic oxyhemoglobin in arterialized venous blood.^{Reference Kameda, Tomizawa and Kawabe2}

Importantly, this signal abnormality can help localize the fistulous point where arterial feeders connect to intracranial veins, a key step in diagnosis and treatment planning. Additionally, SWI may visualize secondary features such as venous congestion and previous hemorrhage, which are critical to understanding the hemodynamic impact of these lesions. Its utility extends to posttreatment follow-up: persistent or recurrent hyperintensity in venous drainage territories may suggest residual or recurrent shunting.^{Reference Letourneau-Guillon and Krings3,Reference Gasparetto, Pires and Domingues4}

Although catheter angiography remains the gold standard for definitive diagnosis and classification of dAVFs, SWI offers a fast, noninvasive screening method that can increase diagnostic suspicion and guide further investigation. In this case, SWI findings correlated with angiographic confirmation of a posterior fossa dAVF, reinforcing its role in the diagnostic work-up of vascular malformations.^{Reference Kameda, Tomizawa and Kawabe2,Reference Chen, Ge and Wan5}