TBI Flashcards
1
Q
Traumatic brain injury (TBI) is a major __ __ __ sustained by __ of people annually
A
public health burden
millions
2
Q
How do you characterize the effects of TBI?
A
clinical severity or underlying pathology
3
Q
What influences expected recovery?
A
clinical severity or underlying patholgy
4
Q
Where was CTE originally found?
A
boxing
5
Q
When are the first clinical signs of CTE typically observed?
A
ones 30s or 40s
6
Q
What characteristic of CTE can be found as early as 20s?
A
focal perivascular clusters of hyperphosphorylated tau - diagnostic of CTE
7
Q
TBI occurs when a __ transmitted to the __ or __ results in __ __
A
force; head; body; neurological dysfunction
8
Q
T/F: in the US alone, an estimated 1.7 million people sustain a TBI
A
true
9
Q
TBI is the leading cause of death and disability for people between the ages _ and _
A
1 to 44 years
10
Q
Discuss the frequency of emergency visits across age groups
A
super high when a child, a lot when youre in your 20s and declines til you 70s
11
Q
What age groups are most likely to sustain a TBI?
A
children aged 0-4, adolescents aged 15-19, adults aged 65+
12
Q
T/F: between the ages of 5 and 25, rates of TBI emergency department visits are approximately two times higher for females compared to males
A
false! males higher
13
Q
What is a major cause of death and disability from TBI?
A
motor vehicle accidents
14
Q
Discuss the frequency of hospitalizations visits across age groups
A
high in your teens, skyrockets in your old age
15
Q
What are the two most commonly used assessment scales for the quantification of TBI?
A
Glasgow coma scale (GCS) score and the duration of loss of consciousness (LOC) or post-traumatic amnesia (PTA), base TBI severity on clinical symptoms
16
Q
What level is a severe TBI score on the glasgow coma scale?
A
3-8
17
Q
What level is a moderate TBI score on the glasgow coma scale
A
9-12
18
Q
What is the glasgow score for a mild tbi?
A
13-15
19
Q
What are the two classifications of TBIs?
A
focal, diffuse
20
Q
What are considered focal injuries?
A
mass lesions, such as contusion, subdural hematoma, and epidural hematoma
21
Q
What are considered diffuse injuries?
A
widely distributed damage, diffuse axonal injury (DAI), hypoxic-ischemic injury, and microvascular injury
22
Q
What are the mortality rates for focal v diffuse injuries?
A
focal - 40%, diffuse 25%
23
Q
List primary focal injuries
A
skull fracture, cortical contusion, focal hemorrhage, intracranial hematoma, focal axonal injury
24
Q
List primary diffuse injuries
A
diffuse axonal injury, petechial hemorrhage, blast injury, excitotoxicity
25
List secondary focal TBIs
microvascular injury, hypoxic-ischemic injury, neuro-inflammation, hypometabolism, edema and herniation, excitotoxicity
26
__ __ are common findings in fatal cases of severe TBI
petechial hemorrhages
27
The main collisions responsible for petechial hemorrhages are...
rapid accelerations and decelerations causing capillary shearing
28
T/F: petechial hemorrhages are not typically visible using most current neuroimaging techniques
true
29
Petechial hemorrhages may coalesce into __ __ with __ __ _
larger lesions; progressive secondary hemorrhage
30
T/F: axonal injury may be diffuse or multifocal, but are often focal
false - they are often diffuse or multifocal but they can be focal
31
The __ of neural tissue allows it to deform in response to normal head movement, and when the human brain is exposed to __ and __, the force may exceed the maximum __ of the __, resulting in DAI
elasticity, rapid acceleration and deceleration, elasticity, tissue
32
After TBI, neurotransmitters, including __, are abruptly __ with massive __ in intracellular calcium, glucose __, kinase __, and __ cerebral blood flow
glutamate
released
increases
hypermetabolism
activation
diminished
33
Describe blast injuries
results from the rapid transmission of an acoustic wave through the brain tissue, along with accompanying blast winds
Blast injuries can be heterogenous and quite different from traumatic impact injury
34
What are the primary pathway by which blast exposure initiates acute brain injury?
blast wind-induced head oscillations at angular accelerations
35
T/F: the resultant cerebral injury in a blast injury is similar to the effects of repetitive concussive impacts
true
36
T/F: primary injuries can be modified with treatment but secondary cannot with TBIs
false, unlike primary injuries, the extent of secondary injuries can be modified via treatment
37
What is one of the most damaging secondary injuries resulting from TBI
progressive secondary hemorrhage
38
T/F: progressive secondary hemorrhage occurs within hours of the TBI and results in the expansion of tissues damage
true
39
Why do progressive secondary hemorrhage injuries cause expansion of tissue damage?
increased intracranial pressure, ischemia, hypoxia, free radical formation, and induction of inflammation
40
__, __, and __ are common secondary events following TBI, and comprise the majority of pre hospitalization secondary injuries in severe TBI
hypotension, hypoxia, ischemia
41
Why are hypoxic-ischemic injuries important target for research?
secondary hypoxic episodes have been established as cuases of death
42
Excessive hypoxemia is associated with __ __
tissue damage
43
The __ and __ __ response to TBI compounds the primary injury
endogenous, exogenous neuroinflammation
44
TBI causes rapid _ __, resulting in the release of __ __ and other __ products that generate free radicals. __ are recruited to phagocytose and clear __ debris after TBI and more __ __ are released
microglial activation, proinflammatory cytokines, neutrophils, cellular, free radicals
45
Free radicals released during neuro-inflammation of TBI cause __ __ and harm otherwise __ __ , thereby propagating __ injury
tissue damage, healthy cells, tissue
46
What imaging techniques have shown evidence of hypometabolism in military veterans and athletes exposed to TBI?
fluorodeoxyglucose positron emission tomography (FDG-PET), fMRI, and animal models
47
Assumed that either __ or __ __ __ is responsible for hypometabolism
DAI, impaired mitochondrial function
48
Studies suggest that __ following TBI is associated with depression and worse prognosis
hypometabolism
49
Secondary brain swelling encompasses both __ and __ and, together with __, is the major contributor to increased __ pressure
edema, congestion, hematomas, intracranial
50
How are edemas caused in TBIs?
TBI alters the permeability of the blood-brain barrier, resulting in altered fluid homeostasis
51
Edemas may eventually lead to __, __, and __ of the brain
distortion, shift, herniation
52
Studies suggest a link between brain trauma and...
AD, Parkinson's, ALS, and CTE
53
After age, family history, and the __ genotype, the risk factor with the strongest linkage to AD is a history of __
ApoE4, TBI
54
Some studies have suggested that TBI is associated with an __ onset of AD
earlier
55
__ and __ have been found in approximately 1/3 of TBI patients who died after TBI, even young people
beta-amyloid plaques, intra-axonal ab deposits
56
Animal models have show that TBI may result in __ __, which results in the Lew bodies characteristic of PD and Lewy body disease
alpha-synuclein deposition
57
T/F: all pathologically diagnosed cases of CTE have come from individuals with a history of minor brain trauma, and that trauma has usually been repetitive
true
58
Not all individuals diagnosed with CTE experienced symptoms after __, suggesting neurological symptoms at the time of injury are __ __ for the development of CTE
acute mild TBI
not necessary
59
Who does CTE typically affect?
athletes or military personnel involved in high-risk activities such as collision or contact sports or military service, and other individuals who are exposed to considerable repetitive brain injury, such as head-banging
60
In addition to boxers, CTE has been identified in...
football players, hockey players, professional wrestlers, military veterans, physically abused individuals, and people with poorly or uncontrolled epilepsy
61
Describe the pathological criteria for the diagnosis of CTE
perivascular foci of p-tau, immunoreactive ATs (astrocytic tangles), and NFTs (neurofibrillary tangle)
irregular cortical distribution of p-tau, immunoreactive NFTs, and ATS with a predilection for the depth of cerebral sulci
clusters of subpial and periventricular ATs in the cerebral cortex, diencephalon, and brainstem
NFTs in the cerebral cortex are located preferentially in the superficial layers
62
What are the gross pathological features of CTE?
generalized cerebral atrophy, with a preference for the frontal, temporal, and medial temporal lobes; enlarged ventricles, thinning of the corpus callosum, cavum septum pellucidum, thinning of the hypothalamic floor, and shrinkage of the mammillary bodies
63
When do the gross pathological features of CTE begin to appear?
changes are not apparent in early stage CTE (I-II), begin to appear in stage III, and are fully evident in stage IV. In most cases, there is also pallor of the locus ceruleus and substantia niagra, which can be severe
64
Describe stage I of CTE
marked by hyperphosphorylated tau restricted to discrete foci in the cerebral cortex, commonly in the superior, dorsolateral, or lateral frontal cortices, as well as perivascularly and at the sulcal depths
65
Describe stage II of CTE
increased p-tau epicenters at the depths of the cerberall sulci and localized spread of neurofibrillary pathology
66
Describe stage III of CTE
p-tau of pathology is widespread; the frontal, insular, temporal, and parietal cortices show neurofibrillary degeneration
amygdala, hippocampus, and entorhinal cortex show neurofibrillary pathology
67
Describe stage IV of CTE
severe p-tau pathology affects most regions of the cerebral cortex and the medial temporal lobe
68
The majority of CTE cases have _ __ __ __ __, with __ pathology, as intraneuronal and intraglial inclusions and neurites found in more than 80% of CTE cases
Tar DNA-binding protein-43
TDP-43
69
T/F: In addition to p-tau pathology, axonal pathology is present at all stages of CTE and appears to progress with stage of CTE
true
70
Neuroinflammation, as seen as __ and activated __ of the __, is a consistent feature of both __ and __
astrocytosis, microglia, white matter
CTE, TBI
71
Where are clusters of microglia found? What is often there?
subcortical white matter
typically a robust astrocytosis
72
__ deposits are found in 40-50% of CTE cases, are significantly associated with age at death, and are not found in the early stages of CTE (I and II)
amyloid-beta peptides
73
__ are found in approximately 20% of CTE cases, and are found in subjects who are significantly older than those without __ __
alpha-synuclein-positive lewy bodies
lewy bodies
74
Describe the clinical symptoms of chronic traumatic encephalopathy
progressive decline in memory and executive function, mood and behavioral disturbances that include depression, apathy, impulsivity, anger, irritability, suicidal behavior, and aggressiveness; gait changes that resemble parkinsonism and progression to dementia eventually
75
What are the two distinct manifestations of CTE?
one that tends to become evident at a younger age with the symptoms of behavioral or mood changes
another that typically manifests later in life with initial symptoms of cognitive impairment
76
Advanced stage CTE is associated with __ __ and dementia is likely by stage __
cognitive impairment, IV
77
What are potential biomarkers for CTE/ TBI?
cerebrospinal fluid
blood
mri
fmri
dti or dai
magnetic resonance spectroscopy
susceptibility weighted imaging
pet
78
What are two potential risk factors for CTE?
apolipoprotein E and gender
79
Apolipoprotein E in boxers and professional football players following a single TBI has been implicated in __ recovery and __ __ performance
prolonged, lower cognitive
80
Most neuropathologically confirmed cases have been identified in __
men
81
T/F: cognitive reserve may also play a role in the development and clinical course of CTE
true; cognitive reserve has been suggested as protective against clinical manifestations, argued it can confer relative resistance to neuropathological changes
