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Background
Up to 20% of strokes are due to intracranial hemorrhage (ICH), and up to 10% of strokes are due to spontaneous ICH (SpICH). SpICH is typically first detected in the emergency department with CT or in short-term follow-up settings with unenhanced MRI. The etiology of SpICH varies based on demographic: older patients experience SpICH from hypertension, cerebral amyloid angiopathy, or hemorrhagic infarction; younger patients experience SpICH from an underlying venous thrombosis, vascular anomaly, or vasculopathy.

Educational Goals / Teaching Points
This educational exhibit aims to outline the pathophysiology and provide characteristic imaging clues of SpICH in patients of an (A) elderly and (B) younger demographic. Through understanding the etiologies of SpICH, a radiologist can communicate the need for additional workup after initial recognition.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
Elderly demographic etiologies: The chronicity of hypertension and cerebral amyloid angiopathy disease processes relate to the elderly demographic predominance. Hypertensive cerebrovascular disease leads to fibrinoid necrosis of small perforating arteries arising from proximal vessels, which over time will weaken vessel walls and predispose patients to vascular ectasia and SpICH. A rapid episodic increase in blood pressure (as is seen with fluid overload, dialysis, or cocaine use), can alternatively lead to SpICH. Hypertensive hemorrhage characteristically occurs in the basal ganglia, thalamus, and cerebellum. Cerebral amyloid angiopathy describes the process of amyloid accumulation in the medium-sized vessels of the parietal or occipital lobes. Amyloid replaces normal vessel wall components, particularly the elastic lamina, which leads to marked vessel fragility through microaneurysm formation and fibrinoid degeneration. Hemorrhagic transformation of an infarct typically occurs after a patient (with a history of infarct) receives thrombolytic therapy. Younger demographic etiologies: Venous thromboses typically occur during dehydration (infants with infection and/or excessive vomiting), hypercoagulable states (autoimmune diseases), acute bacterial infection, and hereditary conditions. These conditions are more often encountered in children, explaining the etiological predominance of SpICH due to venous thromboses in children. Vascular malformations are also encountered in early life and predispose to early intracranial hemorrhage. Examples include arteriovenous malformations and dural arteriovenous fistulas. Vasculitis is characterized by irregular involvement of large or medium vessels with multifocal areas of stenosis and dilation. MR shows multifocal T2 prolongation in the basal ganglia and subcortical white matter.

Conclusion
Follow-up recommendations related to spontaneous intracranial hemorrhage can be improved with an understanding of the pathophysiological basis of the disease. Equipped with this knowledge, the radiologist will be prepared to recommend further angiographic and/or contrast-enhanced MRI when appropriate.