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Radiodiagnosis · Neuroimaging

Indications for neuroimaging in head trauma

The primary goal of diagnostic imaging in traumatic brain injury (TBI) is the prompt identification of life-threatening conditions, such as intracranial hemorrhages, skull base fractures, and vascular injuries. Emergency unenhanced computed tomography (CT) is the first-line imaging modality, allowing for the rapid determination of the need for surgical intervention.

Hematoma densityDecreases by approximately 1 HU per day after the initial hemorrhage
Denver criteriaUsed to determine indications for CT angiography in blunt trauma
HemorrhagesFresh hematomas appear hyperdense on CT with a density of 40–100 HU
Arterial dissectionThe cervical segment of the internal carotid artery proximal to the skull base is most commonly affected
5 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Role of emergency unenhanced CT

Non-contrast CT is used for rapid patient triage: determining who requires emergent neurosurgical decompression (in cases of large hematomas with mass effect) and who requires conservative intensive care. Anatomically, hemorrhages are classified into extracerebral (epidural, subdural, subarachnoid) and intracerebral (intraparenchymal).

Acute intracranial hemorrhage appears hyperdense (increased density, typically 40–100 HU) on CT due to the aggregation of blood cells, platelets, and fibrin. As the clot retracts, its density locally increases due to the hematocrit-raising effect, and then gradually decreases at a rate of ~1 HU per day. In subarachnoid hemorrhage, the formation of a focal hematoma is less likely, as the blood freely mixes with cerebrospinal fluid and disperses.

Denver criteria for vascular imaging

In blunt trauma, the Denver criteria (Denver criteria) are used to determine whether CT or MR angiography should be performed. Angiography is indicated if the patient presents with at least one of the following risk factors:

  • Facial fractures (Le Fort type II or III).
  • Skull base fractures involving the carotid canal.
  • Diffuse axonal injury with a Glasgow Coma Scale (GCS) score < 6.
  • Cervical spine fractures from C1 to C3, subluxations, or involvement of the transverse foramen.
  • History of strangulation asphyxia.

In addition, angiography is indicated in the presence of specific symptoms: arterial bleeding, an enlarging neck hematoma, a vascular bruit in patients under 50 years of age, development of Horner syndrome (Horner syndrome), pulsatile tinnitus, as well as new focal neurological deficit not corresponding to findings on non-contrast CT.

Test your knowledge on the topicTasks from the "Diagnostic Radiology" course bank — instant answers and explanations.

Vascular injuries and arterial dissection

High-energy blunt trauma can cause a vessel to overstretch beyond its mechanical limits. This leads to an int intima tear resulting in arterial dissection (dissection). Blood enters the subintimal space, forming an intramural hematoma that compresses the true vascular lumen. The consequences include restricted blood flow and a high risk of embolic infarctions.

Radiological signs of dissection include:

  • Irregularity of the vessel wall contour.
  • Presence of a detached intimal flap.
  • Intramural hematoma (demonstrating T1 shortening on fat-suppressed T1-weighted MRI sequences).

Complications of vascular injuries may manifest as pseudoaneurysms or arteriovenous fistulas. For example, decompression of hemorrhage into the cavernous sinus leads to the formation of a carotid-cavernous fistula, accompanied by superior ophthalmic vein dilation and exophthalmos.

MRI evolution of hematoma

The MRI signal from an intraparenchymal hemorrhage depends on the temporal evolution of the hematoma and the magnetic properties of the hemoglobin (Hb) molecule:

  1. Hyperacute stage: oxyhemoglobin is present (diamagnetic).
  2. Acute stage: oxygen dissociates, forming deoxyhemoglobin with 4 unpaired electrons (paramagnetic).
  3. Subacute stage: deoxyhemoglobin is oxidized to methemoglobin, with iron transitioning to the ferric state (Fe3+). In the early phase, methemoglobin is intracellular; in the late phase, it is extracellular (due to erythrocyte lysis).
  4. Chronic stage: denatured into hemosiderin (paramagnetic).

Briefly: answers to topical questions

What is the difference between the CT appearance of an epidural hematoma and a subdural hematoma?

The CT appearance of epidural and subdural hematomas differs primarily in shape and their relationship to the anatomical structures of the skull.

SignEpidural hematomaSubdural hematoma
ShapeBiconvex (lentiform)Crescentic (crescentic appearance)
LimitationsDoes not cross cranial suturesBounded by the falx cerebri (falx cerebri)
Relationship to meningesBounded by the dura mater (dura mater)Extends over the cerebral hemisphere surface

In which cases does MRI have an advantage over CT in acute traumatic brain injury?

In acute traumatic brain injury, magnetic resonance imaging has several advantages over computed tomography in assessing parenchymal injury.

  • Detection of hemorrhages — MRI is more sensitive in detecting intracranial hemorrhages at all stages.
  • Diffuse axonal injury (diffuse axonal injury) — MRI is mandatory when DAI is suspected, especially in the presence of a clinico-radiological paradox (when CT findings are minimal).
  • Microbleeds (microbleeds) — T2* or SWI sequences effectively detect microbleeds and hemosiderin deposits.
  • Shear-type injuries (shear-type injuries) — MRI accurately determines their extent.

What complications of head and neck vascular injuries are detected by diagnostic imaging?

Diagnostic imaging of head and neck vascular injuries reveals the following complications:

  • Pseudoaneurysm — a false aneurysm formed when hemorrhage is contained by the adventitia and surrounding tissues.
  • Arteriovenous fistula — rupture of hemorrhage into a venous structure (most commonly a carotid-cavernous fistula, carotico-cavernous fistula).
  • Intramural hematoma — a consequence of arterial dissection leading to compression of the native lumen (native lumen) and embolic infarctions.
  • Dural venous sinus thrombosis — can cause venous infarction, hemorrhage, mass effect, and herniation.
  • Epidural hematomas — in the posterior cranial fossa, they are frequently of venous origin.
  • Complete vessel transection — leads to fatal hemorrhage.
How to memorize

MRI hematoma evolution based on the hemoglobin molecule: "Oh, Give Me Hemoglobin!" — Oxy- (hyperacute), Deoxy- (acute), Methemoglobin (subacute), Hemosiderin (chronic).

Class and exam questions

Why is a dense focal hematoma rarely visible on CT in subarachnoid hemorrhage?

In the subarachnoid space, extravasated blood mixes freely with cerebrospinal fluid and disperses, preventing the formation of a localized dense clot.

In which segment does arterial dissection most commonly occur in blunt neck trauma?

The most vulnerable segment is the cervical internal carotid artery proximal to the skull base, where the artery transitions from a mobile state to a fixed one.

How can dural venous sinus injury be suspected on CT?

Venous sinus rupture may be indicated by a skull base fracture crossing the sinus, as well as the presence of gas bubbles within the sinus lumen (pneumocephalus).

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What else to study on this topic

  • Clivus fractures: classification, mechanism of injury (axial loading), and associated neurological deficits (injury to Dorello's canal).
  • Carotid-cavernous fistula: pathogenesis, early enhancement of ophthalmic veins, and clinical manifestations.
  • Posterior cranial fossa dural sinus injuries: risk of mass effect and herniation.
  • Limitations of CT angiography in trauma: bone artifacts from the skull base and indications for digital subtraction angiography (DSA).
  • Cranial nerve injuries in skull base fractures: jugular foramen and hypoglossal canal.

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