Residency · Residency · Diagnostic Radiology

Intracranial Hemorrhage: Pattern Recognition

Overview

Clinical Significance

Intracranial hemorrhage accounts for approximately 15% of all strokes but more than 40% of stroke mortality. NCCT is the first-line imaging modality and is highly sensitive for acute hemorrhage. Pattern recognition on CT and MRI guides identification of the underlying etiology, with location, morphology, and patient demographics being the keys to differential diagnosis.

CT Appearance of Blood Over Time

In the hyperacute phase (less than 6 hours), blood is isodense to slightly hyperdense and may be missed. In the acute phase (6 hours to 3 days), blood becomes hyperdense at 60-80 HU due to clot retraction. In the subacute phase (3 days to 3 weeks), density progressively decreases from the periphery to the center. In the chronic phase (beyond 3 weeks), blood becomes hypodense or isodense, with encephalomalacia and hemosiderin staining.

MRI Signal of Blood (Key to Aging Hemorrhage)

The MRI signal of blood evolves in a predictable pattern. Hyperacute blood (oxyhemoglobin) is T1 isointense and T2 bright. Acute blood (deoxyhemoglobin) is T1 isointense and T2 dark. Early subacute blood (intracellular methemoglobin) is T1 bright and T2 dark. Late subacute blood (extracellular methemoglobin) is T1 bright and T2 bright. Chronic blood (hemosiderin) is T1 dark and T2 dark with blooming on GRE/SWI.

Epidural Hematoma (EDH)

Key Features

The epidural hematoma has a characteristic biconvex (lenticular) shape and does not cross suture lines. The temporal region is the most common location, resulting from middle meningeal artery injury, with an associated temporal bone fracture in approximately 90% of cases. The classic "lucid interval" describes brief neurologic improvement before rapid deterioration. Most EDH have an arterial source (the middle meningeal artery), though venous EDH can occur in the posterior fossa from dural venous sinus injury and may cross the midline.

Imaging

On CT, the EDH appears as a hyperdense biconvex collection. The "swirl sign" (mixed density within the hematoma) indicates active bleeding. An EDH can cross the midline at the vertex, where the dura is loosely attached. Surgical intervention is indicated when the hematoma exceeds 30 mL, is thicker than 15 mm, or causes more than 5 mm of midline shift.

Subdural Hematoma (SDH)

Key Features

The subdural hematoma has a crescent shape, follows the brain surface, and can cross suture lines but does not cross the midline (limited by the falx). The source is rupture of bridging veins between the cortex and dural venous sinuses. Risk factors include advanced age, anticoagulation, brain atrophy, and trauma (which may be minor). SDH can be bilateral, especially in elderly patients with atrophy.

Imaging by Age

An acute SDH appears as a hyperdense crescent along the inner table. A subacute SDH becomes isodense and may be difficult to see; the radiologist should look for sulcal effacement and midline shift without an obvious collection. A chronic SDH is hypodense and may have internal membranes; it may rebleed, creating a mixed-density appearance. A hygroma is CSF-density, while a chronic SDH may have higher attenuation and membranes.

Special Situations

An acute-on-chronic SDH shows hyperdense acute blood layering within a hypodense chronic collection (the hematocrit effect). An interhemispheric SDH along the falx is associated with child abuse (shaken baby syndrome).

Subarachnoid Hemorrhage (SAH)

Etiologies

Aneurysm rupture is the most common cause of non-traumatic SAH, accounting for approximately 85% of cases. Traumatic SAH commonly appears in the sulci adjacent to a contusion in a convexity distribution. Perimesencephalic (non-aneurysmal) SAH is confined to the perimesencephalic cisterns, carries a benign prognosis, and is CTA negative. Other causes include AVM, vasculitis, coagulopathy, dural AV fistula, and reversible cerebral vasoconstriction syndrome (RCVS).

Imaging

On NCCT, SAH appears as hyperdense material in the subarachnoid spaces (cisterns, sulci, and sylvian fissures). CT sensitivity is approximately 98% within 6 hours but decreases to approximately 90% at 24 hours and approximately 50% at 1 week. If CT is negative and clinical suspicion remains high, lumbar puncture (looking for xanthochromia) or high-resolution MRI (FLAIR is very sensitive) should be obtained. The modified Fisher scale grades the amount and distribution of SAH and predicts the risk of vasospasm. CTA identifies the source aneurysm and may show multiple aneurysms; the ruptured aneurysm is suggested by adjacent hematoma, irregular morphology, or being the largest aneurysm.

Complications

Vasospasm occurs days 3-14 post-SAH and involves narrowing of cerebral arteries that may cause delayed cerebral ischemia. Hydrocephalus may be acute (from blood in the ventricles obstructing CSF flow) or chronic (communicating, from impaired CSF absorption). Rebleeding carries the highest risk in the first 24 hours.

Intraparenchymal Hemorrhage (IPH)

Hypertensive Hemorrhage

Hypertensive hemorrhage is the most common cause of spontaneous IPH. The characteristic locations are the basal ganglia (putamen being most common), thalamus, pons, cerebellum, and subcortical white matter. It results from rupture of small perforating arteries (lenticulostriate and thalamoperforating) affected by chronic hypertensive vasculopathy. It often extends into the ventricles as intraventricular hemorrhage.

Cerebral Amyloid Angiopathy (CAA)

CAA occurs in patients older than 60 and involves deposition of amyloid-beta in cortical and leptomeningeal vessel walls. It produces lobar hemorrhage (cortical/subcortical) in the elderly, with multiple hemorrhages of different ages and recurrent lobar hemorrhage being characteristic. On GRE/SWI, multiple cortical and subcortical microbleeds (punctate foci of susceptibility) and cortical superficial siderosis are seen. Importantly, CAA spares the deep gray matter and brainstem (unlike hypertensive microbleeds). The Boston criteria v2.0 are used for diagnosis.

Hemorrhagic Tumor

Tumors prone to hemorrhage include metastases (melanoma, renal cell, choriocarcinoma, thyroid, and lung) and glioblastoma. Clues to an underlying tumor include surrounding edema disproportionate to the hemorrhage, heterogeneous enhancement, an incomplete hemosiderin ring, multiple lesions, and a known primary malignancy. Follow-up MRI after hematoma resolution may reveal the underlying mass.

Vascular Malformations

An AVM presents as a tangle of vessels (nidus) with enlarged feeding arteries and draining veins, producing susceptibility artifact on GRE/SWI, with the nidus visible on CTA/MRA. A cavernous malformation (cavernoma) has a characteristic "popcorn" appearance on MRI with T1/T2 mixed signal and a hemosiderin rim (blooming on GRE); multiple lesions occur in the familial form, and it is typically occult on angiography. A developmental venous anomaly (DVA) shows a "caput medusae" pattern of radially oriented medullary veins draining into a single collector vein; it is the most common vascular malformation, is benign, and is usually incidental.

Hemorrhagic Transformation of Ischemic Stroke

Hemorrhagic transformation presents as petechial or confluent hemorrhage within an established infarct, occurring 1-7 days after the ischemic event, especially after reperfusion therapy. The location corresponds to a known vascular territory.

Intraventricular Hemorrhage (IVH)

Etiologies

The most common cause of IVH is extension of hypertensive IPH. Other causes include extension of SAH into the ventricles, choroid plexus pathology (vascular malformation or papilloma), and germinal matrix hemorrhage in premature neonates (graded I through IV).

Imaging

IVH appears as hyperdense blood within the ventricle, which may layer dependently. It carries a risk of acute obstructive hydrocephalus, and an external ventricular drain (EVD) may be placed if hydrocephalus develops.

<image>A NCCT panel showing the five major types of intracranial hemorrhage. (1) Epidural hematoma: biconvex hyperdense collection in the temporal region with mass effect and midline shift, limited by the coronal suture. (2) Subdural hematoma: crescent-shaped hyperdense collection crossing the coronal suture. (3) Subarachnoid hemorrhage: hyperdense material filling the basal cisterns and sylvian fissures. (4) Intraparenchymal hemorrhage: hyperdense hematoma in the left putamen (hypertensive) with surrounding edema. (5) Intraventricular hemorrhage: hyperdense blood layering in the occipital horns of the lateral ventricles. Each type is labeled with its characteristic shape and location.</image>

<image>An MRI panel demonstrating cerebral amyloid angiopathy (CAA). Axial SWI (susceptibility-weighted imaging) showing multiple punctate foci of signal loss (microbleeds) distributed in the cortical and subcortical regions of both hemispheres, sparing the deep gray matter (basal ganglia) and brainstem. A FLAIR image shows an acute lobar hemorrhage in the right parietal lobe. A T1-weighted image shows cortical superficial siderosis as a dark line along the cortical surface. Arrows label representative microbleeds, the acute hemorrhage, and cortical siderosis.</image>

<image>A diagram illustrating the common locations of hypertensive intraparenchymal hemorrhage on an axial brain section. Color-coded dots indicate the relative frequency at each site: putamen/basal ganglia (most common, large dot), thalamus, pons, cerebellum, and subcortical white matter. Each location is labeled with the responsible perforating artery (lenticulostriate for putamen, thalamoperforating for thalamus, paramedian pontine perforators for pons). An inset shows a CT image of a classic putaminal hemorrhage with ventricular extension.</image>

Clinical Pearls

Epidural hematomas are biconvex and do not cross suture lines, while subdural hematomas are crescent-shaped and can cross suture lines but do not cross the midline. The "swirl sign" (mixed density within a hematoma) on CT suggests active hemorrhage and is associated with hematoma expansion, making it a surgical emergency. Lobar hemorrhage in an elderly patient should raise suspicion for cerebral amyloid angiopathy, and the radiologist should look for cortical microbleeds and superficial siderosis on SWI. In subarachnoid hemorrhage, CT sensitivity decreases rapidly after 6 hours; if CT is negative but SAH is clinically suspected, lumbar puncture or FLAIR MRI is needed. An underlying mass should always be considered when hemorrhage has disproportionate surrounding edema, an incomplete hemosiderin ring, or heterogeneous enhancement, and follow-up MRI after hematoma resolution is essential. Hypertensive hemorrhage in atypical locations (lobar in a young patient or unusual locations) should prompt investigation for secondary causes such as AVM, tumor, coagulopathy, or drug use.

References

• Hemphill JC, et al. "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage." Stroke (AHA/ASA), 2015
• Greenberg SM, et al. "Cerebral Amyloid Angiopathy: Boston Criteria v2.0." Alzheimer's & Dementia, 2022
• Perry JJ, et al. "Sensitivity of CT within 6 Hours of Symptom Onset for SAH." BMJ, 2011
• ACR Appropriateness Criteria: Cerebrovascular Disease, 2019

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