Specific Imaging Findings

The imaging modality in the acute setting is usually CT, which reveals hyperdense mass typically in one of the following locations: basal ganglia, thalamus, central pons, and medial cerebellum. It is primarily the location that allows for hypertensive hematoma characterization on imaging, as blood products have the same appearance irrespective of the etiology. A clot forms after the extravasation of blood, with progressively increasing density over the first 3 days, caused by clot retraction with extrusion of the hypodense serum. This low attenuation surrounding the clot increases in size with development of vasogenic edema. Ring contrast enhancement may be observed around the hematoma. Hypertensive hematomas typically dissect the brain without a considerable amount of associated tissue necrosis, so that chronic lesions are transformed into slit-like hypodense cavities, with a rim of very low T2 signal caused by hemosiderin deposition. MRI is more sensitive than CT for parenchymal hemorrhage, primarily with T2*-weighted images, which frequently demonstrate additional multifocal small hypointensities, corresponding to hemosiderin from previous microhemorrhages. Contrast extravasation on CTA, known as spot sign, predicts hematoma expansion.

Pertinent Clinical Information

Hypertensive bleeds more commonly occur in males, on average at around 55 years of age. Rapid elevation of blood pressure is the main predisposing factor, and drugs such as cocaine and amphetamine are commonly responsible in younger individuals. The presenting symptoms depend on the location: confusion and hemiparesis in basal ganglia and thalamus, cranial nerve deficits and coma in pons, and nausea and vomiting in cerebellum.