Role of MRI in Traumatic Brain Injury

Dr Hardik D Patel2nd year resident doctorRadiology departmentNHL Medical college, Ahmedabad

Introduction Craniocerebral injuries are the common cause of hospital admission

following trauma High morbidity and mortality particularly in adolescent and young adults Traumatic brain injury: 2 categories1. Primary injury Initial injury to the brain as a result of direct trauma Example: hematoma, diffuse axonal injury, contusion2. Secondary injury Subsequent injury to the brain after the initial insult Result from systemic hypotension, hypoxia, elevated intracranial

pressure (ICP) or biochemical insults

Clinically, this classification is important because secondary injuries can be preventable, whereas primary injuries, by definition, have already occurred by the time the patient first presents for medical attention.

IntroductionImaging is critical to both the diagnosis and management of TBI.For diagnosis of TBI in the acute setting, noncontrast CT is the

modality of choice as it quickly and accurately identifies intracranial hemorrhage that warrants neurosurgical evacuation. CT readily identifies both extra-axial hemorrhage (epidural, subdural, and subarachnoid/intraventricular hemorrhage) and intra-axial hemorrhage (cortical contusion, intraparenchymal hematoma, and TAI or shear injury).

While CT is the mainstay of TBI imaging in the acute setting, magnetic resonance imaging (MRI) has better diagnostic sensitivity for certain types of injuries that are not necessarily hemorrhagic, including cortical contusions and nonhemorrhagic traumatic axonal injuries.

Role of MRIMagnetic resonance imaging (MRI) is recommended

for patients with acute TBI when the neurologic findings are unexplained by CT.

MR is also the modality of choice for subacute or chronic injury.

MR is Sensitive for detection of diffuse axonal injury or contusion with susceptibility sequence (T2 gradient echo)

MR is more sensitive to subtle extra-axial collections, non-hemorrhagic lesions, brainstem injuries, and subarachnoid hemorrhage (SAH) when using fluid-attenuated inversion recovery (FLAIR).

Diffuse Axonal InjuryFrequent cause of persistent vegetative state and

morbidity in traumatic brain injury patientsEtiology-pathogenesisTraumatic deceleration injury: shearing/rotational

forces in areas of greater density differential in the brain (= grey-white matter interface)

Can be an isolated finding in traumatic brain injuryNo (or little) association with presence of

subarachnoid, subdural hemorrhage, or skull fracture

Diffuse Axonal InjuryClinical featuresUsually results in instantaneous loss of consciousness.

Clinical symptoms worse than CT findingsMost patients (90%) remains in vegetative state (rarely

causes death because brainstem function typically unaffected)

General imaging featuresCan be either hemorrhagic or non-hemorrhagic (the latter

is more common)Grey-white matter interface, brain stem, corpus callosumNumber and location of lesions predict prognosis (worst

when multiple, and in supratentorial location)

Diffuse Axonal InjuryCT findingsMay be normal (microscopic, nonhemorrhagic

lesions can be missed by CT)Small hemorrhagic foci in typical locationsMR findingsMRI is the imaging of choice to detect DAISusceptibility sequence needed for detection of

hemorrhagic DAI (called T2 GRE, or T2*). Hemorrhagic lesions will be dark.

Non-hemorrhagic lesions are bright on T2-WI and FLAIR

Diffuse Axonal InjuryImaging recommendation for suspected DAIWhen initial brain CT is normal but the

patient is in vegetative stateMRI with susceptibility sequence ORFollow up brain CT in 24 hours (1/6 of DAI

will evolve, may be seen in subsequent CT)

MR with susceptibility sequence/Gradient echo imaging (T2 GRE)Gradient-echo imaging is highly sensitive to

local magnetic inhomogeneity caused by the presence of blood.

Hemosiderin, a breakdown product of blood, is ferromagnetic. The presence of hemosiderin alters the local magnetic susceptibility of tissue, resulting in areas of signal loss on gradient echo T2*-weighted images.

Because hemosiderin can persist indefinitely, its detection on gradient-echo T2*-weighted images allows for improved evaluation of remote injury.

Axial CT image shows mild diffusebrain swelling without intracranialhemorrhage. Small subgalealhematoma is present (red arrow).

Same day MRI (Susceptibilitysequence) shows multiple tiny areas ofblood products (red arrows) in the greywhitematter junctions and deep greynuclei consistent with DAI. Blue arrowrepresents a vascular flow void.

Small interpeduncular SAH and petechial hemorrhage in dorsolateral midbrain on CT and susceptibility-weighted MRI

DAI on CT and MR. In Grade II DAI, the corpus callosum is injured. Note the low attenuation within the splenium of thecorpus callosum on CT (A). The FLAIR image demonstrates abnormalhyperintensity in the same region (B). The diffusion-weighted image (DWI) shows a focus of bright signal intensity (C). The T2*-weighted image gradient-echo image shows scattered foci of susceptibility staining (signal loss) (D).

SWI

Cerebral ContusionClassic location: anterior base of frontal and

temporal lobesMultiple, bilateralCan be normal earlyCan be non-hemorrhagicMRI is better for detection, delineating extents

of contusions

Hemorrhagic contusion (red arrows) at the frontal bases, rightmore than left, is noted as an ill-defined area of hypodensity inCT and high signal intensity zone in MRI T2-WI. MRI is moresensitive to depict the extent of this injury.

Middle aged man, fall from height

Cortical contusion near the skull base. (A) Sagittal T1-weighted image demonstrates abnormal T1 shortening (increasedsignal intensity) involving the right orbitofrontal lobe. There is associateddecreased signal on the gradient-echo images due to thepresence of hemosiderin (B). The FLAIR (C) and T2-weighted (D)images demonstrate mixed heterogenous signal due to a combinationof methemoglobin, hemosiderin, and edema. Small bilateraltemporal contusions are also noted.

No SAH is seen on CT, but on MRI, SAH is well visualized

Comparison of CT and FLAIR MRI in Traumatic SAH

No SAH is seen on CT, but on MRI, SAH is well visualized

Single sulcal SAH seen on CT, but on MRI FLAIR multiple sulcal hemorrhages are seen

SAH is seen at a single site on CT scan but on both sides in multiple sulci on MRI FLAIR image

MRI appearances of hemorrhage at different stage

• The MR appearance of a haemorrhage evolves over time, depending on the biochemical state of hemoglobin. • Acute hemorrhage MRI － iso-intensity on T1WI, slightly low or low intensity on T2WI( ideally MR is poor than CT for Acute hemorrhage ).• Sub acute hemorrhage MRI － iso- or high signal intensity on T1WI, iso- or slightly high signal intensity on T2WI.• Chronic hemorrhage MRI － high signal intensity both on T1WI/T2WI.

Subacute SDH

Isodense subacute SDH. During the transition from acute tochronic SDH, an isodense phase occurs. At this stage, the SDH(arrowhead) can be difficult to discriminate from the adjacent parenchyma.

Axial T1-weighted magnetic resonance imaging demonstrates bilateral subacute subdural hematomas with increased signal intensity. Areas of intermediate intensity represent more acute hemorrhage into the subacute collections.

T2-weighted magnetic resonance imaging in a patient with subdural hematoma shows blood products of differing ages.

Appearance of the chronic SDH on MRI. The chronic SDH is always slightly higher in signal intensity than CSF on T1-weighted, fluid attenuation inversion recovery (FLAIR) imaging and proton-density MR images. It is hypointense to gray and white matter on T1-weighted images (A), and hyperintense to brain parenchyma on T2-weighted images (B-D).

Conclusion…..MRI is more sensitive than CT for detection of diffuse

axonal injury, contusions or subtle SAH using susceptibility sequence (T2 gradient echo), DWI and FLAIR

MRI is helpful in distinguishing different ages of haemorrhage i.e. to know how old the haemorrhage is.

Limitations• Certain absolute contraindications, e.g. pacemaker,

ferromagnetic foreign bodies• Lower sensitivity for bone fractures and hyperacute blood• Difficult managing trauma patients in MRI suite: metallic

life support, monitoring device• Longer imaging time (than CT)

Thank you…