Traumatic brain injury

Question 1

Two major classifications of head trauma?

Answer 1

Primary injuries and complications, vs 2ndary complications from the primary injury.

Question 2

Define primary injury

Answer 2

consequence of brain damage occurring at impact. It may result in contusions of the brain and DAI

Question 3

List 5 secondary complications of TBI

Answer 3

(1) raised intracranial pressure (ICP), leading to increased cerebral edema and hydrocephalus
(2) hypoxia
(3) infection and (4) infarction secondary
to or in addition to (5) brain herniation

Question 4

What cistern do you look for to be obliterated to predict risk for elevated ICP?

Answer 4

mesencephalic cistern

Question 5

How often do patients experience limited mental effects from an epidural hematoma, and what is this period called?

Answer 5

50%, lucid interval

Question 6

Most common cause(s) of epidural hematoma?

Answer 6

Temporal bone fracture with disruption of the middle meningeal artery or vein.

Tears of the middle meningeal artery (60% to 90%) or venous structures (middle meningeal vein, venous sinus, or diploic veins; 10% to 40%) result in the extravasation of blood and acute epidural hematoma.

Question 7

Cause and mechanism of subdural hematoma?

Answer 7

Acute subdural hematomas result from significant head injury and are caused by the shearing of bridging veins
This occurs because of rotational movement of the brain with respect to fixation of these veins at the adjacent venous sinus or dura. (penetrating injury also a cause)

Question 8

Term for post-traumatic hemorrhage in a lobe of the brain?

Answer 8

“burst lobe”

Question 9

Types of subdural hematoma?

Answer 9

simple (without associated brain parenchymal injury) and complicated (with parenchymal injury).

Question 10

% of severe closed head trauma with SDH, and % mortality rate

Answer 10

30% of patients with severe closed head trauma

associated with a 35% to 50% mortality rate

Question 11

One of the most important clinical factors affecting outcome of SDH (and most traumas)?

Answer 11

Control of ICP

Question 12

Time frames for acute, subacute and chronic SDH?

Answer 12

Lesions occurring at the time of the initial injury are considered acute, although symptoms may take up to a few days to become manifest

Those lesions becoming symptomatic between approximately 3 days to 3 weeks are subacute

those lesions that are diagnosed after 3 weeks are considered chronic.

Question 13

Density of acute, subacute and chronic SDH?

Answer 13

Acute - high (exceptions: anemia, DIC, ongoing
bleeding, or tears in the arachnoid membrane leading to dilution)

Subacute - Subacute subdural hematomas, on the other hand, are usually isodense to low density. Subacute and chronic subdural lesions enhance due to vascularization of the subdural membranes. Repeated episodic bleeding results in fibrous septations and compartments within the hematoma. Subacute and chronic subdural hematomas may also display layering.

Chronic - usually low density. High and low density levels observed in these lesions may be caused by rebleeding into the chronic subdural collection.

Question 14

Causes of chronic SDH in infants?

Answer 14

birth injury, vitamin K deficiency, coagulopathy, or child abuse.

Question 15

How is contrast helpful in identifying iso-dense SDH?

Answer 15

Contrast is helpful in isodense subdural hematoma by visualizing the inwardly displaced cortical veins

Question 16

Causes of subdural hygroma?

Answer 16

can result from trauma and can either occur acutely as a tear in the arachnoid membrane with CSF collecting in the subdural space or can result from the chronic degradation of a subdural hematoma.

Question 17

How do you tell the difference between cerebral atrophy and subdrual hygroma?

Answer 17

cortical veins. In atrophy they course through the space, in hygroma they are displaced medially and do not course through.

Question 18

What MR features make the diagnosis of hygroma a “slam-dunk?”

Answer 18

being able to discern high protein (bright on FLAIR) and small amounts of residual hemorrhage (gradient echo).

Question 19

Besides trauma, what else may cause a subdural hygroma?

Answer 19

intracranial hypotension (spontaneous) or acquired.

Question 20

Definition of brain contusion

Answer 20

brain parenchymal bruises where petechial hemorrhage (because of the gray matter vascularity) is visualized in the cortex.

Question 21

What is a contrecoup contusion?

Answer 21

whereas diametrically opposed contusions, i.e. occuring opposite the side of external truma

Question 22

CT appearances of brain contusion?

Answer 22

high density is noted at the site of injury.

Focal regions of low density representing edema surround the acute hemorrhage.

Question 23

Where do the most severe cases of diffuse axonal injury (DAI) typically occur?

Answer 23

regions include the body (usually lateralized to

one side and on the inferior surface) and the splenium (most common location) of the corpus callosum.

Question 24

pathological progression of DAI?

Answer 24

Within days axonal swelling (retraction ball) develops, within weeks microglial clusters are observed, and within months wallerian degeneration takes place.

Question 25

CT appearance of DAI?

Answer 25

On CT, one may visualize focal punctate regions of high density that may be surrounded by a collar of low-density edema. These are hemorrhagic shearing injuries most likely associated with complete axonal disruption. On CT, it may be difficult to detect nonhemorrhagic shearing injury early.

Question 26

MR appearance of DAI?

Answer 26

MR reveals high intensity on T2WI/FLAIR, which may or may not be associated with hemorrhage Eighty percent of DAI lesions are nonhemorrhagic. Both hemorrhagic and nonhemorrhagic shearing injuries are easily visualized by MR. Lesions may be ovoid or elliptic, with the long axis parallel to fiber bundle directions.

Question 27

What are the 5 patterns of brain herniation?

Answer 27

inferior tonsillar and cerebellar herniation, superior vermian herniation (upward herniation), temporal lobe/uncal herniation, central transtentorial herniation, and subfalcine herniation.

Question 28

What do you call compression of the contralateral cerebral peduncle against the edge of the tentorium
by a supratentorial mass, producing ipsilateral motor weakness?

Answer 28

Kernohan-Woltman notch phenomenon (false localizing sign)

Question 29

What nerve gets compressed most often with transtentorial herniation? What symptom does this cause?

Answer 29

Oculomotor. Ipsilateral papillary dilation.

Question 30

What lobar anatomy herniates with tentorial herniation?

Answer 30

Uncus of the temporal lobe

Question 31

What vessels are compressed with tentorial herniation causing vascular infraction along the distribution of these arteries?

Answer 31

posterior cerebral and anterior choroidal arteries

Question 32

What do you call hemorrhages in the tegmentum of the

pons and the midbrain caused by uncal herniation?

Answer 32

Duret hemorrhages.

Question 33

What vessels may be compressed with a subfalcine herniation?

Answer 33

anterior cerebral artery or internal cerebral veins

Question 34

What is the most common intracranial vascular dissection?

Answer 34

the supraclinoid part of the internal carotid, midway between the cavernous carotid and bifurcation. Dissection may extend into the anterior or middle cerebral artery.

Question 35

Mortality rate of intracranial vascular dissection?

Answer 35

75%

Question 36

What sign is seen on angiography with a disected internal crotid (showing an irregular, narrowed carotid with a tapered configuration)

Answer 36

“string sign”

Question 37

Skull fractures that raise suspicion for child abuse?

Answer 37

depressed fractures with a history of “mild trauma,” fractures that cross the midline, and those involving the occiput without a known significant event.
epi/sub dural hematomomas of various age as well, etc.

Question 38

What is “white cerebellum sign”?

Answer 38

When there is diffuse low density of the cerebral cortex and basal ganglia, typically secondary to hypoxia.

Question 39

What are the 3 patterns seen with hypoxic injury from global oligemia (strangling).

Answer 39

In pattern I the lesions are confined to the watershed zones, in pattern III lesions involve the cortex and basal ganglia diffusely, and pattern II has some combination of I and III.

Question 40

4 general categories of skull fractures?

Answer 40

linear, diastatic, comminuted, and depressed.

Question 41

Describe the pathophysiology of a leptomeningeal cyst.

Answer 41

When the dura is torn with the skull fracture, the arachnoid can insinuate itself into the cleft of the fracture. When the pulsations of the CSF enlarge the cleft between the fracture fragments, it produces either linear widening of the fracture margins or multiloculated cysts with smooth, scalloped margins.