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Brain: Imaging, Pathology, and Anatomy > Chapter 2: Primary Effects of CNS trauma (Scalp and Skull Injuries; Extraaxial Hemorrhages) > Flashcards

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

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1
Q

What is direct trauma?

A

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.

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2
Q

What is the cause of indirect trauma?

A

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.

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3
Q

What are the five layers of the scalp?

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

Scalp injuries include _____ and _____.

A

Lacerations and hematomas

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5
Q

Wood fragments are?

a. Hypodense
b. Isodense
c. Hyperdense

A

A. Hypodense

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6
Q

Density of leaded glass, gravel, and metallic shards?

A

Variably hyperdense

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7
Q

What are the two distinctly different types of scalp hematomas?

A

Cephalohematomas and subgaleal hematomas.

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8
Q

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.

A

Cephalohematomas

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9
Q

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.

A

Cephalohematomas

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10
Q

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.

A

Cephalohematomas

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11
Q

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

A

Cephalohematomas

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12
Q

Complications of cephalohematoma.

A

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.

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13
Q

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

A

Subgaleal hematomas

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14
Q

Blood collects under the aponeurosis of the occipitofrotalis muscle.

A

Subgaleal hematomas

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

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15
Q

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.

A

Subgaleal hematomas

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16
Q

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

A

Subgaleal hematomas

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17
Q

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

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

LIPS - N

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18
Q

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

A

Linear skull fracture

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

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19
Q

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.

A

Depressed skull fracture

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20
Q

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.

A

Depressed skull fracture

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21
Q

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.

A

Elevated skull fracture

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22
Q

A fracture that widens a suture or synchondrosis.

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

A

Diastatic skull fracture

“diastases” or “splits open”

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23
Q

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

Why?

A

It typically does not ossify completely until mid teens.

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24
Q

Most common site of diastatic skull fractures.

A

Sphenooccipital synchondrosis.

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25
Q

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

A

“Growing” skull fracture

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26
Q

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

A

Stage I

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

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27
Q

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

A

Stage II

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28
Q

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.

A

Stage II

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29
Q

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

A

Stage III

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30
Q

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.

A

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.

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31
Q

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

A

Epidural hematomas

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32
Q

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

A

Subdural hematomas

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33
Q

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

A

Subarachnoid hemorrhage

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34
Q

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

A

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

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35
Q

In EDH location. 90% are ____ and _____.

A

Unilateral and supratentorial.

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36
Q

Epidural hematoma:

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

A

The squamous portion of the temporal bone.

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37
Q

Intracranial hematoma that:

  • Biconvex in shape
  • Rarely cross the suture lines
A

Epidural hematoma

38
Q

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

A

If a fracture traverses the suture or sutural diastasis.

39
Q

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?

A

Indicates active, rapid bleeding with unretracted clot.

40
Q

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

A

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

41
Q

MR findings of EDHs

A

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

42
Q

Possible finding of angiography (DSA) in EDHs.

A

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.

43
Q

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

A

Venous epidural hematoma

44
Q

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

A

Venous epidural hematoma

45
Q

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.

A

Vertex epidural hematoma

46
Q

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

A

Anterior temporal epidural hematoma

47
Q

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

A

Anterior temporal epidural hematoma

48
Q

What vessel is injured in anterior temporal epidural hematoma?

A

Sphenoparietal dural venous sinus

  • as it curves medially along the undersurface of the lesser sphenoid wing, extravasting blood into the epidural space.
49
Q

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

A

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

50
Q

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.

A

Clival epidural hematoma

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

51
Q

Most commonly affected nerve in clival EDH?

A

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.

52
Q

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

A

Clival EDH

53
Q

Management of clival EDH is dictated by what?

A

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

54
Q

What is more common, subdural hematoma or epidural hematoma?

A

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.

55
Q

Most common cause of acute subdural hematoma?

A

Trauma

56
Q

Most common etiology of acute subdural hematoma?

A

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

57
Q

Less common causes of aSDH include?

A

Aneurysm rupture

Skull/dura-arachnoid metastases from vascular extracranial primary neoplasms

Spontaneous hemorrhage in patients with severe coagulopathy

58
Q

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

A

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.

59
Q

Surveillance with follow-up CT scans is recommended until the SDH resolves.

OR at least up to how many weeks following initial trauma?

A

5 weeks

60
Q

What is the classic finding of acute subdural hematoma?

A

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

61
Q

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

A

Subdural hematoma

62
Q

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

A

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

63
Q

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

A

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.

64
Q

Finding of aSDH in perfusion CT.

A

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.

65
Q

MR finding in acute SDH?

A

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.

66
Q

What is the use of CTA in acute subdural hematoma?

A

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

67
Q

The major differential diagnosis of subdural hematoma is epidural hematoma.

What are the main differences?

A

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

68
Q

How old is a subacute subdural hematoma?

A

Between several days and several weeks old.

*No specific numbers mentioned

69
Q

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

A

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.

70
Q

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

A

1-2 HU each day.

An SDH will become nearly isodense with the underlying cerebral cortex within a few days following trauma.

71
Q

MR findings of subacute subdural hematoma.

A

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).

72
Q

What is the most sensitive standard sequence for detecting sSDH?

A

FLAIR

73
Q

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

A

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

74
Q

What is the major differential diagnosis of an sSDH?

A

Isodense acute SDH.

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

75
Q

Other differential diagnoses for sSDH?

A

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.

76
Q

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

A

Chronic subdural hematoma (cSDH)

77
Q

Percentage of rehemorrhage in chronic subdural hematoma?

A

5 - 10%

78
Q

What is the pathology regarding rehemoorhage in chronic subdural hematoma?

A

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.

79
Q

Noncontrast CT finding of an uncomplicated chronic subdural hematoma.

A

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.

80
Q

What is “armored brain”?

A

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”.

81
Q

Contrast-enhanced CT finding for chronic subdural hemorrhage.

A

The encapsulating membranes around the cSDH contain fragile neocapillaries that lack endothelial tight junctions.

Therefore, the membranes show strong enhancement following contrast administration.

82
Q

MR findings of chronic subdural hemorrhage.

A

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.

83
Q

Differential diagnoses for chronic subdural hemorrhage.

A

Simple brain atrophy with enlarged bifrontal CSF spaces.

Subdural hygroma.

Subdural effusion.

Subdural empyema.

84
Q

What is the most common cause of intracranial subarachnoid hemorrhage?

A

Trauma

NOT RUPTURED SACCULAR ANEURYSM

85
Q

Traumatic subarachnoid hemorrhage is predominantly found in what location?

A

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

86
Q

Terson syndrome is associated with traumatic subarachnoid hemorrhage.

What is Terson syndrome?

A

Intraocular hemorrhage

87
Q

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

A

Acute traumatic subarachnoid hemorrhage

88
Q

Typical finding of traumatic subarachnoid hemorrhage on MR?

A

“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.

89
Q

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

A

With the exception of location

Adjacent to cortical contusions
Superficial sulci > basilar cisterns

90
Q

Major differential diagnosis of traumatic subarachnoid hemorrhage?

A

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.

91
Q

Sulcal-cisternal hyperintensity on FLAIR is seen in subarachnoid hemorrhage, however, it is nonspecific.

What are the other causes of sulcal-cisternal hyperintensity?

A

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

92
Q

What is pseudosubarachnoid hemorrhage?

A

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.

Brain: Imaging, Pathology, and Anatomy (5 decks)

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