Intracranial hematomas, collections of blood within the skull, are critical conditions often resulting from head injuries. Understanding their specific characteristics through neuroimaging is paramount for accurate diagnosis and timely treatment. This article provides a comprehensive overview of the neuroimaging of intracranial hematomas, detailing how different types appear on CT and MRI scans, a crucial topic for students of medicine and related fields.

Neuroimaging of Intracranial Hematomas: An Overview

Neuroimaging plays a vital role in identifying, characterizing, and monitoring intracranial hematomas. These imaging techniques allow clinicians to distinguish between different types of bleeding based on their location, shape, density/signal intensity, and how they evolve over time. This differentiation is key to determining the underlying cause and the most appropriate management.

Subdural Hematomas: Imaging Features and Evolution

Subdural hematomas (SDH) typically originate from the stretching or tearing of cortical veins that bridge the subdural space. They are often associated with acute deceleration injuries like motor vehicle accidents or falls, and frequently co-occur with cortical contusions and diffuse axonal injury (DAI).

Acute Subdural Hematoma Imaging

On axial CT, acute subdural hematomas appear as crescent-shaped extra-axial collections with high attenuation. They are commonly found along the convexity, falx, and tentorium. Key characteristics include:

Shape: Crescent-shaped on axial CT. MR can reveal a lentiform or biconvex appearance in the coronal plane, differentiating them from the typical CT presentation.
Location: Most are supratentorial, along the convexity, falx, and tentorium.
Dural Reflections: SDHs do not cross dural reflections like the falx cerebri or tentorium. However, they can cross sutural margins and frequently layer along the entire hemispheric convexity.
Density (CT): Initially hyperdense (50-60 HU relative to normal brain at 18-30 HU) due to clot retraction. Occasionally, they can be isodense or hypodense in severe anemia or with active extravasation.
Mass Effect: Diffuse swelling of the underlying hemisphere is common, potentially leading to more mass effect than expected by the collection's size, and little reduction in midline shift post-evacuation.
MRI: Acute SDHs show excellent contrast difference on FLAIR imaging, appearing hyperintense against hypointense calvarium.

Subacute and Chronic Subdural Hematoma Imaging

The appearance of subdural hematomas changes significantly over time:

Isodense Phase: Usually occurs several days to 3 weeks after the acute event. The hematoma itself is less conspicuous on noncontrast CT. Indirect signs include sulcal effacement, white matter buckling, a thick gray matter mantle, ventricular distortion, and midline shift.
Postcontrast CT: May show peripheral enhancement of the collection, indicating subacute injury.
T1WI (MRI): High signal intensity caused by methemoglobin distinguishes subacute SDHs from non-hemorrhagic fluid collections.
T2WI (MRI): The T2 signal increases as the hemorrhage ages.
Chronic SDH (CT): Low attenuation values, similar to CSF, making differentiation from prominent subarachnoid space due to cerebral atrophy challenging. Contrast enhancement can help by demonstrating an enhancing capsule or displaced cortical veins.
Chronic SDH (MRI): As the hemorrhage ages, T1 signal gradually decreases. Chronic hematomas appear on T2WI as well as T1WI (refer to source for Figure 3.11).
Rebleeding: Can cause a heterogeneous appearance due to a mixture of fresh blood and partially liquefied hematoma. A sediment level or “hematocrit effect” may be seen.

Epidural Hematomas: Distinctive Imaging Characteristics

Epidural hematomas (EDH) are typically arterial in origin, often resulting from a skull fracture disrupting the middle meningeal artery. They can also occur from stretching or tearing of meningeal arteries without a fracture, especially in children. Skull fractures are present in 85-95% of cases.

Acute Epidural Hematoma Imaging

On CT, acute epidural hematomas present with a classic appearance:

Shape: Well-defined, high attenuation lenticular or biconvex extra-axial collections.
Location: Most are temporal or temporoparietal, though frontal and occipital can occur. Venous EDHs are less common, often located at the vertex, posterior fossa, or anterior middle cranial fossa.
Cause: Primarily arterial (e.g., middle meningeal artery disruption). Venous EDHs result from disrupted dural venous sinuses.
Dural Attachment: EDHs strip the dura from the inner table of the skull. They generally do not cross cranial sutures where the dura is firmly attached. However, vertex epidurals, usually venous, can cross the midline (sagittal sinus). They are external to and not bounded by dural reflections like the tentorium.
Associated Findings: Mass effect, sulcal effacement, and midline shift are frequently seen. Bone windows often show an overlying linear skull fracture.
Heterogeneous Appearance: Irregular areas of lower attenuation may indicate active extravasation of fresh, unclotted blood, requiring immediate surgical attention.
MRI: On T2WI, acute EDHs appear as biconvex low signal collections, with the dura visible as a thin black line deep to the collection, confirming its epidural location.

Subarachnoid Hemorrhage: Detecting Bleeding in the CSF Space

Subarachnoid hemorrhage (SAH) is common in head injuries, resulting from disrupted small subarachnoid vessels or direct extension from contusions/hematomas. It rarely causes significant mass effect. SAH can also indicate a ruptured aneurysm in unwitnessed events.

Imaging Subarachnoid Hemorrhage

CT: Appears as linear areas of high attenuation within the cisterns and sulci. Small amounts of blood might only cause apparent effacement of sulci. Convexity or tentorial SAH can be differentiated from SDH by its extension into adjacent sulci.
MRI: Traditionally harder to detect hyperacute SAH on conventional T1W/T2W MRI, as it can be isointense to brain parenchyma. However, FLAIR and SWI are more sensitive than CT in detecting acute subarachnoid blood, with SAH appearing hyperintense on FLAIR and markedly hypointense on SWI.
Subacute SAH (MRI): Better appreciated due to high signal intensity when blood might be isointense to CSF on CT.
Chronic SAH (MRI): May show hemosiderin staining (

Neuroimaging of Intracranial Hematomas