An 18-year-old man presented to the neurosurgery outpatient department with recurrent episodes of epistaxis for the past 8 years and altered behavior for the past month. Epistaxis was scanty in amount, intermittent, spontaneous, and not associated with any trauma or nasal obstruction or breathing difficulties. Bleeding used to stop spontaneously after some time. There was no history of associated headache, seizures, vomiting, fever, or loss of consciousness. On physical examination, the patient was afebrile, with normal vital signs and normal Glasgow Coma Scale score (15 of 15) at the time of presentation. Multiple dilated engorged veins were visible on the forehead; however, there was no evidence of abnormal skin pigmentation. Neurologic examination yielded findings that were within normal limits. Laboratory examinations revealed a hemoglobin level of 11 g/dL (normal range, 13.2–16.6 g/dL), with the rest of the parameters within normal limits. This patient underwent unenhanced CT of the brain and paranasal sinuses followed by contrast-enhanced MRI of the brain for further evaluation (Figs 1–3).Unenhanced CT of the brain revealed a well-defined hyperattenuated tortuous structure in the suprasellar region and left temporal lobe (Fig 1). Contrast-enhanced MRI of the brain was performed. Axial T2-weighted MRI revealed multiple serpiginous flow voids in the left gangliothalamic region, with prominent flow void in the deep cerebral vein and left cortical vein. A few transosseous and subcutaneous flow voids are also seen in the frontal region (Fig 2). Gadolinium-enhanced T1-weighted images showed multiple enhancing tangles of vessels in the entire left cerebral hemisphere, with interspersed normal brain parenchyma. There was no evidence of prominent dominant feeders; however, multiple small feeders were seen arising from the internal carotid artery, anterior cerebral artery, and posterior cerebral artery. Multiple transosseous feeders were seen arising from the external carotid artery (Fig 3A). A large dilated tortuous venous varix was seen in the left suprasellar region, draining via the left cortical veins into the superior sagittal sinus and left transverse sinus (Fig 3B, 3D). Multiple enhancing clustered vascular channels were seen extending via the cribriform plate into the left nasal cavity (Fig 3C). The clinical history and constellation of neuroimaging findings were indicative of cerebral proliferative angiopathy. The diagnosis was confirmed with conventional digital subtraction angiography. Lateral oblique angiogram of the left internal carotid artery (Fig 4A, 4B) revealed a large poorly defined nidus in the left cerebral hemisphere, with persistent scattered puddling of contrast material in the late arterial and venous phases. There was no evidence of dominant arterial feeders. No intranidal aneurysm was seen. An early draining venous varix was noted, draining via the cortical veins into the superior sagittal sinus and left transverse sinus. Anteroposterior angiogram of the left internal carotid artery (Fig 4C) revealed multiple clustered vascular channels extending into the left nasal cavity. Initially, this case was managed conservatively; however, there was no remarkable improvement in this patient’s condition. He has refused to undergo endovascular embolization of extracranial vessels for control of epistaxis. What is your diagnosis?