CNS Trauma Flashcards

1
Q

Secondary CNS injury mechanisms includes the activation of the coagulation cascade, with VEGF release, which has this effect on vascular permeability

A

Increased

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2
Q

In cerebral edema, neuronal death causes cell fragmentation/dissolution, leading to areas of this

A

Hyperosmolarity

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3
Q

Mass effect of hematoma expansion includes these 2 things

A

Induced ischemia and Vasogenic edema

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4
Q

In cerebral edema, what leads to areas of hyperosmolarity?

A

Neuronal death that causes cell fragmentation/dissolution

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5
Q

Injury due to trauma/shaking with temporary impairment but no focal findings
Due to neuronal stretching and injury
Clinical: headache, confusion, loss of consciousness, dizzy, no measurable residual defect

A

Concussion

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6
Q

Concussion injures this part of neurons

A

Axons

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7
Q

Diffuse pattern of neuronal traumatic injury with axonal shearing
Requires large amount of force, often rotational force
Result is shearing or twisting of axons

A

Diffuse axonal injury

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8
Q

Most diffuse axonal injuries occur in these brain regions

A

White matter tracts
(corpus callosum, brain stem, CB peduncles)

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9
Q

Large amount of force, especially rotational force, can cause this type of neuronal injury

A

Diffuse axonal injury
(shearing or twisting of axons)

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10
Q

Is there loss of consciousness with concussion?

A

Yes

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11
Q

Is there loss of consciousness with diffuse axonal injury?

A

Immediate loss or decreased consciousness

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12
Q

With this CNS injury, imaging shows only focal small hemorrhages and edema, especially in the corpus callosum and midbrain

A

Diffuse axonal injury

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13
Q

Severe diffuse axonal injury leads to this

A

Death or permanent vegetative state

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14
Q

Milder diffuse axonal injury leads to this

A

Cognitive or physical disability

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15
Q

At 24 hours with this CNS injury, you begin to see axonal swelling and retraction bulbs

A

Diffuse axonal injury

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16
Q

Retraction bulbs (swollen endings at the tips of injured axons) are seen morphologically 24 hours after this CNS injury

A

Diffuse axonal injury

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17
Q

Is gliosis seen in diffuse axonal injury?

A

Yes, if the patient survives

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18
Q

Neurodegenerative disorder due to repetitive head trauma (seen in athletes, military, abuse victims)

A

Chronic traumatic encephalopathy

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19
Q

Chronic traumatic encephalopathy is also known as this

A

Dementia pugilistica

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20
Q

Dementia pugilistica is another name for this condition

A

Chronic traumatic encephalopathy

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21
Q

Neurofibrillary tangles are seen in this condition

A

Chronic traumatic encephalopathy

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22
Q

Neurofibrillary tangles are seen in Chronic traumatic encephalopathy, due to this protein becoming abnormally phosphorylated

A

Tau protein

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23
Q

In Chronic traumatic encephalopathy, abnormally phosphorylated tau protein forms this

A

Neurofibrillary tangles

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24
Q

In Chronic traumatic encephalopathy, phosphorylated tau proteins (and neurofibrillary tangles) interfere with this function and transport
May be directly toxic and result in neuronal death

A

Microtubule

25
Perivascular neuronal/astrocytic accumulation of Phospho-tau is seen in this condition
Chronic traumatic encephalopathy
26
Phosphorylated tau proteins are found at depths of sulci in Chronic traumatic encephalopathy with this relation to vasculature
Perivascular
27
This condition is IHC positive for phosphoryalted Tau protein
Chronic traumatic encephalopathy
28
This CNS injury can cause mood disorders, suicidal ideation, cognition/memory problems, pyramidal defects, and dysarthria
Chronic traumatic encephalopathy
29
This is a "bruise" of the brain
Cerebral contusion
30
Cerebral contusion is most common at these locations of the brain
Bony prominences of frontal and temporal bones
31
Cerebral contusion is most common at bony prominences of these 2 bones
Frontal and temporal bones
32
This describes a cerebral contusion that occurs on the side of trauma impact
Coup lesion
33
This describes a cerebral contusion that occurs on the side opposite of trauma impact
Contrecoup lesion
34
Morphologically, cerebral contusions occur here
At top of gyri
35
Hemorrhage, necrosis and edema are seen morphologically early or late after cerebral contusion?
Early
36
Hemosiderin and gliosis are seen morphologically early or late after cerebral contusion?
Late (brown, depressed soft lesions; siderophages; reactive astrocytes; loss of neuropil)
37
This type of skull fracture is a fracture through suture line
Diastatic fracture
38
This type of skull fracture may result in leptomeningeal cyst and suture line separation
Diastatic fracture
39
This type of skull fracture often does not require intervention
Simple linear non-depressed fracture
40
A basilar skull fracture to this compartment can cause CSF rhinorrhea and raccoon eyes
Anterior
41
A basilar skull fracture to this compartment can cause Battle sign (bruising behind the ear), CSF otorrhea, and hemotypamun
Posterior
42
This protein is found in CNS, and can be detected in CSF rhinorrhea that occurs from anterior basilar skull fracture
Beta-2 transferrin
43
Beta-2 transferrin is found in this
CSF
44
A patient with raccoon eyes may have had this type of CNS injury
Basilar skull fracture (anterior)
45
A patient with bruising behind their ear and blood in their ear cavity may have had this type of CNS injury
Basilar skull fracture (posterior)
46
Do basilar skull fractures have good outcomes?
No; relatively poor outcomes
47
How does perinatal brain injury correlate with gestational age?
Increases inversely with gestational age
48
Subependymal periventricular zone of tissue with stem cells and immature glial tissue Loose vasculature without supporting basement membrane or vascular media Vulnerable to high pressure or hypoxic states
Germinal matrix
49
The germinal matrix is located near this, in inferior wall of lateral ventricles
Thalamus
50
Germinal matrix is located near the thalamus, in the inferior wall of this
Lateral ventricles
51
Germinal matrix is prominent at this gestational time; regresses in infancy
2nd / 3rd trimester
52
Is germinal matrix hemorrhage usually serious?
Usually clinically silent (may produce sudden deterioration if large enough - decerebrate posturing, stupor, apnea)
53
Aqueductal stenosis, subarachnoid obliteration, and periventricular white matter degeneration are possible sequelae of this condition
Germinal matrix hemorrhage
54
Germinal matrix hemorrhage may cause the obliteration of this
Subarachnoid
55
Group of permanent disorders of movement due to non-progressive disturbances of developing brain
Cerebral palsy
56
Is cognition affected in cerebral palsy?
Often not affected
57
Are patients with cerebral palsy born with a complicated labor and delivery?
No (Most born with uncomplicated labor and delivery)
58
Does perventricular leukomalacia, a lesion that can cause cerebral palsy, have symmetric or focal clinical findings?
Symmetric (e.g. spastic di/quadriplegia)