Chapter 2: Primary Effects of CNS trauma (Scalp and Skull Injuries; Extraaxial Hemorrhages)

Question 1

What is direct trauma?

Answer 1

Involves a blow to the head and is usually caused by automobile collisions, falls, or injury inflicted by an object such as hammer or baseball bat.

Scalp lacerations, hematomas, and skull fractures are common.

Question 2

What is the cause of indirect trauma?

Answer 2

Angular kinematics

Typically occurs in high-speed motor vehicle collisions. Here the brain undergoes rapid deformatio and distortion.

Depending on the site and direction of the force applied, significant injury to the cortex, axons, penetrating blood vessels, and deep gray nuclei may occur.

Question 3

What are the five layers of the scalp?

Answer 3

1. Skin,
2. Subcutaneous fibrofatty tissue
3. Galea aponeurotica
4. Loose areolar connective tissue
5. Periosteum

Question 4

Scalp injuries include _____ and _____.

Answer 4

Lacerations and hematomas

Question 5

Wood fragments are?

a. Hypodense
b. Isodense
c. Hyperdense

Answer 5

A. Hypodense

Question 6

Density of leaded glass, gravel, and metallic shards?

Answer 6

Variably hyperdense

Question 7

What are the two distinctly different types of scalp hematomas?

Answer 7

Cephalohematomas and subgaleal hematomas.

Question 8

These hematomas are subperiosteal blood collections that line in the potential space BETWEEN the outer surface of the CALVARIUM and the PERICRANIUM, which serves as the periosteam of the skull.

Answer 8

Cephalohematomas

Question 9

These are the extracranial equivalent of an intracranial epidural hematoma.

They do not cross the suture lines and typically unilateral.

Because they are anatomically constrained by the tough fibrous periosteum and its insertion, they rarely attain a large size.

Answer 9

Cephalohematomas

Question 10

These occur in 1% of newborns and are more common following instrumental delivery. They are often diagnosed clinically but imaged only if they are unusually prominent or if intracranial injuries are suspected.

Answer 10

Cephalohematomas

Question 11

NECT scans show a somewhat lens-shaped soft tissue mass that overlies a single bone (usualy the parietal or occipital bone)

Answer 11

Cephalohematomas

Question 12

Complications of cephalohematoma.

Answer 12

Rare. Most resolve spontaneously over a few days or weeks.

Occasionally the elevated periosteum at the periphery of a chronic cephalohematoma undergoes dystrophic calcification, creating a firm palpable mass.

Question 13

These hematomas are subaponeurotic collections and are common findings in traumatized patients for all ages.

Answer 13

Subgaleal hematomas

Question 14

Blood collects under the aponeurosis of the occipitofrotalis muscle.

Answer 14

Subgaleal hematomas

Lies deep to the scalp muscles and galeal aponeurotica but external to the periosteum, it is not anatomically limited by suture lines.

Question 15

Bleeding can be very extensive. They are usually bilateral lesions that often spread diffusely around the entire calvaria.

NECT scan shows a heterogeneous hyperdense cresentic scalp mass that crosses one or more suture lines.

Answer 15

Subgaleal hematomas

Question 16

Most of these hematomas resolve without treatment. However, expanding hematomas in infants and small children can cause significant blood loss.

Answer 16

Subgaleal hematomas

Question 17

Tramatized patient should have a dedicated facial CT if what physical examination finding is present?

Answer 17

1. Lip laceration
2. Intraoral laceration
3. Periorbital contusion
4. Subconjunctival hemorrhage
5. Nasal laceration

LIPS - N

Question 18

Type of fracture that is a sharply marginated linear defect that typically involves the inner and outer tables of the calvaria.

Answer 18

Linear skull fracture

Most are caused by relatively low-energy blunt trauma that is delivered over a relatively wide surface area.

Question 19

Fracture in which the fragments are displaced inward.

Comminution of the fracture fragments starts at the point of maximum impact and caused by high-energy direct blows to a small surface with a blunt-object.

Answer 19

Depressed skull fracture

Question 20

These fractures tear the underlying dura and arachnoid and are associated with cortical contusions and potential leakage of CSF into the subdural space.

Fractures extending to a dural sinus or the jugular bulb are associated with venous sinus thrombosis in 40% of cases.

Answer 20

Depressed skull fracture

Question 21

Theses fractures are usually caused by long, sharp object (such as a machete or propeller) that fractures the calvaria, simulataneously lifting and rotating the fracture fragment.

Answer 21

Elevated skull fracture

Question 22

A fracture that widens a suture or synchondrosis.

Usually occur in associated with a linear skull fracture that extends into an adjacent suture.

Answer 22

Diastatic skull fracture

“diastases” or “splits open”

Question 23

Traumatic diastasis of the sphenoocipital, petrooccipital and/or occipitomastoid synchondroses is common in children with severely comminuted central skull base fractures.

Why?

Answer 23

It typically does not ossify completely until mid teens.

Question 24

Most common site of diastatic skull fractures.

Answer 24

Sphenooccipital synchondrosis.

Question 25

This is also known as "posttraumatic leptomeningeal cyst" or "craniocerebral erosion".

Answer 25

"Growing" skull fracture

Question 26

Stage of growing skull fracture in which it extends from the time of initial injury to just before the fracture enlarges.

Answer 26

Stage I Early recognition and dural repair of stage I GSFs produce the best result.

Question 27

Stage of growing skull fracture that lasts for approximately 2 months following initial fracture enlargement.

Answer 27

Stage II

Question 28

Stage of growing skull fracture in which the bone defect is small, skull deformity is relatively limited, and neurologic deficits are mild. The entrapped tissue prevents normal fracture healing.

Answer 28

Stage II

Question 29

Stage of growing skull fracture that begins 2 months after the initial enlargement begins.

Answer 29

Stage III

Question 30

Stage of growing skull fracture in which the bone defect becomes significantly larger. Brain tissue and CSF extend between the bony edges of the fracture through the torn dura and arachnoid.

Answer 30

Stage III Patients with late-stage GSF often present months or even years after head trauma. Stage GSFs can cause pronounced skull deformities and progressive neurologic deficits if left untreated.

Question 31

Hematomas that arise between inner table of the skull and outer (periosteal) layer of the dura.

Answer 31

Epidural hematomas

Question 32

Hematomas located between the inner (meningeal) layer of the dura and the arachnoid.

Answer 32

Subdural hematomas

Question 33

Hematomas found within the sulci and subarachnoid cisterns, between arachnoid and the pia.

Answer 33

Subarachnoid hemorrhage

Question 34

The vast majority of epidural hematomas (EDH) are caused by what?

Answer 34

Caused by arterial injury (90%). Most commonly to the middle meningeal artery.

Question 35

In EDH location. 90% are ____ and _____.

Answer 35

Unilateral and supratentorial.

Question 36

Epidural hematoma: 90- 95% are found directly adjacent to a skull fracture. What is the most common site?

Answer 36

The squamous portion of the temporal bone.

Question 37

Intracranial hematoma that: - Biconvex in shape - Rarely cross the suture lines

Answer 37

Epidural hematoma

Question 38

10% of EDH in children DO CROSS the sutures, in what cases?

Answer 38

If a fracture traverses the suture or sutural diastasis.

Question 39

The classic imaging appearance of classic (arterial) EDHs is a hyperdense (60-90 HU) biconvex extraaxial collection. Presence of a hypodense component ("swirl" sign) is seen in about 1/3 of cases. What does it indicate?

Answer 39

Indicates active, rapid bleeding with unretracted clot.

Question 40

In acute epidural hematoa: what imaging findings are associated with adverse clinical outcome?

Answer 40

Thickness > 1.5 cm Volume of > 30 mL Pterional (lateral aspect of the middle cranial fossa) location Midline shift > 5 mm Presence of "swirl" sign

Question 41

MR findings of EDHs

Answer 41

Acute EDHs are typically isointense with underlying brain, especially on T1W1. The displaced dura can be identified as displaced "black line: between the hematoma and the brain

Question 42

Possible finding of angiography (DSA) in EDHs.

Answer 42

DSA may show a lacerated middle meningeal artery with "tram-track" fistulization of contrast from the middle meningeal artery into the paired middle meningeal veins. Mass effect with displaced cortical arteries and veins is seen.

Question 43

Type of epidural hematoma that are often smaller, are under low pressure, and develop more slowly.

Answer 43

Venous epidural hematoma

Question 44

Type of EDH that can "straddle" intracranial compartments, crossing both sutures and lines of dural attachment and compressing or occluding the adjacent venous sinsues.

Answer 44

Venous epidural hematoma

Question 45

This hematoma is usually caused by a linear or diastatic fracture that crosses the superior sagittal sinus, they often accumulate over hours or even days with slow, subtle onset of symptoms.

Answer 45

Vertex epidural hematoma

Question 46

Unique subgroup of hematomas that occur in the anterior tip of the middle cranial fossa.

Answer 46

Anterior temporal epidural hematoma

Question 47

This hematoma is caused either by an isolated fracture of the adjacent greater sphenoid wing or bu an isolated zygomaticomaxillary complex ("trpio") facial fracture.

Answer 47

Anterior temporal epidural hematoma

Question 48

What vessel is injured in anterior temporal epidural hematoma?

Answer 48

Sphenoparietal dural venous sinus - as it curves medially along the undersurface of the lesser sphenoid wing, extravasting blood into the epidural space.

Question 49

The anterior temporal epidural hematoma typically remain stable in size and do not require surgical evacuation. Why?

Answer 49

Because it is limited anatomically by the sphenotemporal suture laterally and the orbital fissure medially.

Question 50

This hematoma usually develop after a hyperflexion or hyperextension injury to the neck and are possibly caused by stripping of the tectorial membrane attachements to the clivus.

Answer 50

Clival epidural hematoma Less commonly, they have been associated with basilar skull fractures that lacerate the clival dural venous plexus.

Question 51

Most commonly affected nerve in clival EDH?

Answer 51

The abducens nerve is most commonly affected, followed by the glossopharyngeal and hypoglossal nerves. They are typically limited in size by the right attachment of the dura to the basisphenoid and tectorial membrane.

Question 52

EDH that most often occur in children and present with multiple cranial neuropathies.

Answer 52

Clival EDH

Question 53

Management of clival EDH is dictated by what?

Answer 53

By severity and progression of the neurologic deficits and stability of the ATLANTOAXIAL JOINT.

Question 54

What is more common, subdural hematoma or epidural hematoma?

Answer 54

Subdural hematoma Most do not occur as isolated injuries; the vast majority of SDHs are associated with traumatic subarachnoid hemoorhage as well as significant parenchymal injuries such as cortical contusions, brain lacerations, and diffuse axonal injuries.

Question 55

Most common cause of acute subdural hematoma?

Answer 55

Trauma

Question 56

Most common etiology of acute subdural hematoma?

Answer 56

Tearing of bridging cortical veins as they cross the subdural space to enter a dural venous sinus (usually the superior sagittal sinus),

Question 57

Less common causes of aSDH include?

Answer 57

Aneurysm rupture Skull/dura-arachnoid metastases from vascular extracranial primary neoplasms Spontaneous hemorrhage in patients with severe coagulopathy

Question 58

Is it possible that subdural hemorrhage can be of arterial origin?

Answer 58

Yes. Tearing of cortical arteries from skull fracture may also give rise to an aSDH. Rarely, an acute spontaneous aSDH of arterial origin occurs in someone without any traumatic history of vascular anomaly. These patients usually have sudden serious disturbance of consciousness and have a poor outcome unless the aSDH is recognized and treated promptly.

Question 59

Surveillance with follow-up CT scans is recommended until the SDH resolves. OR at least up to how many weeks following initial trauma?

Answer 59

5 weeks

Question 60

What is the classic finding of acute subdural hematoma?

Answer 60

Supratentorial crescent-shaped extraaxial collection that displaces the gray-white matter interface medially.

Question 61

Hematoma that crosses the suture lines but generally do not cross dural attachment.

Answer 61

Subdural hematoma

Question 62

Mortality is very high in subdural hematoma in what CT scan finding?

Answer 62

If the difference between the midline shift and thickness of the hematoma is 3 mm or more, then mortality is very high.

Question 63

An aSDH is nearly isodense with the underlying cortex in what cases?

Answer 63

Found in extremely anemic patients (Hgb under 8-10 g/dL) and sometimes occurs in patients with coagulopathy. In rare cases, CSF leakage through a torn arachnoid may mix with - and dilute- the acute blood that collects in the subdural space.

Question 64

Finding of aSDH in perfusion CT.

Answer 64

CT or xenon perfusion scans may demonstrate decreased cerebral blood flow (CBF) and low perfusion pressure, which is one of the reasons for the high mortality rate of patients. The cortex underlying an evacuated aSDH may show hyperemic changes with elevated rCBF values. Persisting hyperemia has been associated with poor outcome.

Question 65

MR finding in acute SDH?

Answer 65

Isointense on T1WI and hypointense on T2WI. Signal intensity on FLAIR scans is usually iso- to hyperintense compared with CSF but hypointense compared with the adjacent brain. aSDH are hypointense on T2* scans. DWI shows heterogeneous signal within the hematoma but may show patchy foci of restricted diffusion in the cortex underlying the aSDH.

Question 66

What is the use of CTA in acute subdural hematoma?

Answer 66

May be useful in visualizing a cortical vessel that is actively bleeding into the subdural space.

Question 67

The major differential diagnosis of subdural hematoma is epidural hematoma. What are the main differences?

Answer 67

Shape: SDH - Cresentic, EDH - Biconvex EDH = almost always associated with fracture; SDH = frequently occur in the absence of skull fracture EDH = may cross sites of dural attachement; SDHs = do not cross the falx of tentorium

Question 68

How old is a subacute subdural hematoma?

Answer 68

Between several days and several weeks old. | *No specific numbers mentioned

Question 69

Within 2-3 days, what happens to subdural hematoma?

Answer 69

The initial soft, loosely organized clot of an acute SDH becomes organized. Breakdown of blood products and the formation of organizing granulation tissue change the imaging apperance of subacute and chronic SDHs.

Question 70

Density of extraaxial hematoma decreases approximately how many HU each day?

Answer 70

1-2 HU each day. An SDH will become nearly isodense with the underlying cerebral cortex within a few days following trauma.

Question 71

MR findings of subacute subdural hematoma.

Answer 71

Early sSDH - isointesen with cortex on T1WI and hypointense of T2WI but gradually become more hyperintense as extracellular methemoglobin incraeses. Late-stage sSDH are T1/T2 "bright-bright" FLAIR: early sSDH may initially appear hypointense due to their intrinsic T2 shortening. T2*: sSDH show distinct "blooming" DWI: Cresentic high-intensety area with low-intensity rim closer to the brain surface (*double layer" appearance).

Question 72

What is the most sensitive standard sequence for detecting sSDH?

Answer 72

FLAIR

Question 73

DWI in sSDH shows a double layer appearance which represents what?

Answer 73

Low-intensity area corresponds to a mixture of resolved clot and CSF, whereas the high-intensity area correlated with solid clot.

Question 74

What is the major differential diagnosis of an sSDH?

Answer 74

Isodense acute SDH. Which are typically seen only in an extremely anemic or anticoagulated patient.

Question 75

Other differential diagnoses for sSDH?

Answer 75

Subdural effusion - that follows surgery or menignitis or that occurs as a component of intracranial hypotension can mimic an sSDH. Subdural hygroma - typically isodense/isointense with CSF and does not demonstrate enhancing, encapsulating membranes.

Question 76

This hematoma is an encapsulated collection of sanguieous or serosanguineous fluid confined within the subdural space.

Answer 76

Chronic subdural hematoma (cSDH)

Question 77

Percentage of rehemorrhage in chronic subdural hematoma?

Answer 77

5 - 10%

Question 78

What is the pathology regarding rehemoorhage in chronic subdural hematoma?

Answer 78

Organization and resorption of the hematoma contained wtihin the "membranes" of surrounding granulation tissue continue. These neomembranes have FRAGILE, EASILTY DISRUPTED CAPILLARIES AND EASILY REBLEED, creating a mixed subdural hematoma.

Question 79

Noncontrast CT finding of an uncomplicated chronic subdural hematoma.

Answer 79

A hypodense crescentic fluid collection extending over the surface of one or both cerebral hemispheres. Approach CSF in density. Hematocrit effect creates a slight gradation in density that increases from top to bottom.

Question 80

What is "armored brain"?

Answer 80

With age, the encapsulating membranes surrounding the cSDH become thickened and may appear moderately hyperdense. Eventually, some cSDHs show peripheral calcifications that persist for many years. In rare cases, a cSDH may densely calcify or even ossify, a condition aply termed "armored brain".

Question 81

Contrast-enhanced CT finding for chronic subdural hemorrhage.

Answer 81

The encapsulating membranes around the cSDH contain fragile neocapillaries that lack endothelial tight junctions. Therefore, the membranes show strong enhancement following contrast administration.

Question 82

MR findings of chronic subdural hemorrhage.

Answer 82

T1: iso- to slight hyperintense compared with CSF T2: isop to hypointense compared with CSF FLAIR: Hyperintense T2*: "blooming" if subacute-chronic blood clots are present. Encapsulating membranes of cSDH enhance following contrast administration. Typically, the outer layer is thicker than the inner layer. DWI: Uncomplicated cSDH do not restrict on DWI.

Question 83

Differential diagnoses for chronic subdural hemorrhage.

Answer 83

Simple brain atrophy with enlarged bifrontal CSF spaces. Subdural hygroma. Subdural effusion. Subdural empyema.

Question 84

What is the most common cause of intracranial subarachnoid hemorrhage?

Answer 84

Trauma NOT RUPTURED SACCULAR ANEURYSM

Question 85

Traumatic subarachnoid hemorrhage is predominantly found in what location?

Answer 85

Predominantly found in the perisylvian regions, in the anteroinferior frontal and temporal sulci, and over the hemispheric convexities.

Question 86

Terson syndrome is associated with traumatic subarachnoid hemorrhage. What is Terson syndrome?

Answer 86

Intraocular hemorrhage

Question 87

Hemorrhage that is typically peripheral, appearing as linear hyperdensities in sulci adjacent to cortical contusions or under epi- or subdural hyematomas.

Answer 87

Acute traumatic subarachnoid hemorrhage

Question 88

Typical finding of traumatic subarachnoid hemorrhage on MR?

Answer 88

"Dirty" sulci with "smudging" of the perisylvian cisterns. Subarachnoid blood is hyperintense to brain on TwWI and appears similar in signal to cisternal CSF. FLAIR = hyperintensity T2* = Blooming GRE or SWI = hypointense signal intensity surrounded by hyperintense CSF DWI = foci of restricted diffusion in areas of frank ischemia or trauma-induced cytotoxic edema.

Question 89

General imaging apperance of traumatic subarachnoid hemorrhage is similar to that of aneurysmal subarachnoid hemorrhage, with what exception?

Answer 89

With the exception of location Adjacent to cortical contusions Superficial sulci > basilar cisterns

Question 90

Major differential diagnosis of traumatic subarachnoid hemorrhage?

Answer 90

Nontraumatic subarachnoid hemorrhage Anuerysmal rupture causes 80-90% of ntSAH. Arteriovascular malformnations account for 10-15% of nt SAH. Dissections and dissecting aneurysms, especially of the vertebrobasilar system, are less common but important causes of ntSAH.

Question 91

Sulcal-cisternal hyperintensity on FLAIR is seen in subarachnoid hemorrhage, however, it is nonspecific. What are the other causes of sulcal-cisternal hyperintensity?

Answer 91

Meningitis, neoplasm, artifact (incomplete CSF supression), contrast leakage into the subarachnoid space (e.g. with renal failure), and high inspired oxygen during general anesthesia.

Question 92

What is pseudosubarachnoid hemorrhage?

Answer 92

Term used to described the CT appearance of a brain with severe cerebral edema. Hypodense brain makes circulating blood in arteries and veins look relatively hyperdense. The hyperdensity seen here is smooth and conforms to the expected shape of the vessels, not the subarachnoid spaces, and should not be mistekaed for tSAH or ntSAH.