IntroductionIntracranial calcifications are frequently observed in radiological examinations and are generally benign. Subcortical white matter calcifications however warrant further clinical and radiological investigation due to potential associations with infections, metabolic and inherited disorders like Sturge-Weber Syndrome and Fahr disease (1). One rare cause of subcortical calcification would be dural arteriovenous fistula (DAVF), where abnormal connections form between dural venous sinuses, cortical, or leptomeningeal veins, and arterial feeders often from meningeal or scalp arteries (2). DAVFs account for 10-15% of intracranial vascular malformations (3). The etiology of DAVFs remains controversial. Acquired factors like dural venous sinus thrombosis and trauma are linked to adult-onset cases, while congenital factors likely underlie DAVFs presenting in pediatric patients (4). The most common location for DAVF is at the transverse-sigmoid junction, with a slight left-sided predominance (6). Radiologically, DAVFs with chronic venous hypertension or reflux are associated with intracranial hemorrhage or focal areas of cerebral edema (7).As of now, only seven case reports of subcortical white matter calcifications associated with DAVF have been documented. These cases show variability in the distribution of intracranial calcifications, including focal lobar calcifications, unilateral supratentorial brain, bilateral symmetrical supratentorial brain, and basal ganglia calcifications (8-14). In this case study, we present a 57-year- with new symmetric subcortical white matter calcifications within the supratentorial brain and dentate nuclei. These calcifications developed over 2 years on a background of untreated DAVF with chronic venous hypertension. This case study emphasizes the potential morbidity associated with untreated dural arteriovenous fistula (DAVF) over an extended period.