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Neurobiology of Adult Brain Disorders > TBI > Flashcards

TBI Flashcards

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1
Q

Traumatic brain injury (TBI) is a major __ __ __ sustained by __ of people annually

A

public health burden
millions

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2
Q

How do you characterize the effects of TBI?

A

clinical severity or underlying pathology

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3
Q

What influences expected recovery?

A

clinical severity or underlying patholgy

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4
Q

Where was CTE originally found?

A

boxing

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5
Q

When are the first clinical signs of CTE typically observed?

A

ones 30s or 40s

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6
Q

What characteristic of CTE can be found as early as 20s?

A

focal perivascular clusters of hyperphosphorylated tau - diagnostic of CTE

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7
Q

TBI occurs when a __ transmitted to the __ or __ results in __ __

A

force; head; body; neurological dysfunction

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8
Q

T/F: in the US alone, an estimated 1.7 million people sustain a TBI

A

true

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9
Q

TBI is the leading cause of death and disability for people between the ages _ and _

A

1 to 44 years

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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

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11
Q

What age groups are most likely to sustain a TBI?

A

children aged 0-4, adolescents aged 15-19, adults aged 65+

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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

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13
Q

What is a major cause of death and disability from TBI?

A

motor vehicle accidents

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14
Q

Discuss the frequency of hospitalizations visits across age groups

A

high in your teens, skyrockets in your old age

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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

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16
Q

What level is a severe TBI score on the glasgow coma scale?

A

3-8

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17
Q

What level is a moderate TBI score on the glasgow coma scale

A

9-12

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18
Q

What is the glasgow score for a mild tbi?

A

13-15

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19
Q

What are the two classifications of TBIs?

A

focal, diffuse

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20
Q

What are considered focal injuries?

A

mass lesions, such as contusion, subdural hematoma, and epidural hematoma

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21
Q

What are considered diffuse injuries?

A

widely distributed damage, diffuse axonal injury (DAI), hypoxic-ischemic injury, and microvascular injury

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22
Q

What are the mortality rates for focal v diffuse injuries?

A

focal - 40%, diffuse 25%

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23
Q

List primary focal injuries

A

skull fracture, cortical contusion, focal hemorrhage, intracranial hematoma, focal axonal injury

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24
Q

List primary diffuse injuries

A

diffuse axonal injury, petechial hemorrhage, blast injury, excitotoxicity

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25
Q

List secondary focal TBIs

A

microvascular injury, hypoxic-ischemic injury, neuro-inflammation, hypometabolism, edema and herniation, excitotoxicity

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26
Q

__ __ are common findings in fatal cases of severe TBI

A

petechial hemorrhages

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27
Q

The main collisions responsible for petechial hemorrhages are…

A

rapid accelerations and decelerations causing capillary shearing

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28
Q

T/F: petechial hemorrhages are not typically visible using most current neuroimaging techniques

A

true

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29
Q

Petechial hemorrhages may coalesce into __ __ with __ __ _

A

larger lesions; progressive secondary hemorrhage

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30
Q

T/F: axonal injury may be diffuse or multifocal, but are often focal

A

false - they are often diffuse or multifocal but they can be focal

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31
Q

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

A

elasticity, rapid acceleration and deceleration, elasticity, tissue

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32
Q

After TBI, neurotransmitters, including __, are abruptly __ with massive __ in intracellular calcium, glucose __, kinase __, and __ cerebral blood flow

A

glutamate
released
increases
hypermetabolism
activation
diminished

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33
Q

Describe blast injuries

A

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
Q

What are the primary pathway by which blast exposure initiates acute brain injury?

A

blast wind-induced head oscillations at angular accelerations

35
Q

T/F: the resultant cerebral injury in a blast injury is similar to the effects of repetitive concussive impacts

A

true

36
Q

T/F: primary injuries can be modified with treatment but secondary cannot with TBIs

A

false, unlike primary injuries, the extent of secondary injuries can be modified via treatment

37
Q

What is one of the most damaging secondary injuries resulting from TBI

A

progressive secondary hemorrhage

38
Q

T/F: progressive secondary hemorrhage occurs within hours of the TBI and results in the expansion of tissues damage

A

true

39
Q

Why do progressive secondary hemorrhage injuries cause expansion of tissue damage?

A

increased intracranial pressure, ischemia, hypoxia, free radical formation, and induction of inflammation

40
Q

__, __, and __ are common secondary events following TBI, and comprise the majority of pre hospitalization secondary injuries in severe TBI

A

hypotension, hypoxia, ischemia

41
Q

Why are hypoxic-ischemic injuries important target for research?

A

secondary hypoxic episodes have been established as cuases of death

42
Q

Excessive hypoxemia is associated with __ __

A

tissue damage

43
Q

The __ and __ __ response to TBI compounds the primary injury

A

endogenous, exogenous neuroinflammation

44
Q

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

A

microglial activation, proinflammatory cytokines, neutrophils, cellular, free radicals

45
Q

Free radicals released during neuro-inflammation of TBI cause __ __ and harm otherwise __ __ , thereby propagating __ injury

A

tissue damage, healthy cells, tissue

46
Q

What imaging techniques have shown evidence of hypometabolism in military veterans and athletes exposed to TBI?

A

fluorodeoxyglucose positron emission tomography (FDG-PET), fMRI, and animal models

47
Q

Assumed that either __ or __ __ __ is responsible for hypometabolism

A

DAI, impaired mitochondrial function

48
Q

Studies suggest that __ following TBI is associated with depression and worse prognosis

A

hypometabolism

49
Q

Secondary brain swelling encompasses both __ and __ and, together with __, is the major contributor to increased __ pressure

A

edema, congestion, hematomas, intracranial

50
Q

How are edemas caused in TBIs?

A

TBI alters the permeability of the blood-brain barrier, resulting in altered fluid homeostasis

51
Q

Edemas may eventually lead to __, __, and __ of the brain

A

distortion, shift, herniation

52
Q

Studies suggest a link between brain trauma and…

A

AD, Parkinson’s, ALS, and CTE

53
Q

After age, family history, and the __ genotype, the risk factor with the strongest linkage to AD is a history of __

A

ApoE4, TBI

54
Q

Some studies have suggested that TBI is associated with an __ onset of AD

A

earlier

55
Q

__ and __ have been found in approximately 1/3 of TBI patients who died after TBI, even young people

A

beta-amyloid plaques, intra-axonal ab deposits

56
Q

Animal models have show that TBI may result in __ __, which results in the Lew bodies characteristic of PD and Lewy body disease

A

alpha-synuclein deposition

57
Q

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

A

true

58
Q

Not all individuals diagnosed with CTE experienced symptoms after __, suggesting neurological symptoms at the time of injury are __ __ for the development of CTE

A

acute mild TBI
not necessary

59
Q

Who does CTE typically affect?

A

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
Q

In addition to boxers, CTE has been identified in…

A

football players, hockey players, professional wrestlers, military veterans, physically abused individuals, and people with poorly or uncontrolled epilepsy

61
Q

Describe the pathological criteria for the diagnosis of CTE

A

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
Q

What are the gross pathological features of CTE?

A

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
Q

When do the gross pathological features of CTE begin to appear?

A

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
Q

Describe stage I of CTE

A

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
Q

Describe stage II of CTE

A

increased p-tau epicenters at the depths of the cerberall sulci and localized spread of neurofibrillary pathology

66
Q

Describe stage III of CTE

A

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
Q

Describe stage IV of CTE

A

severe p-tau pathology affects most regions of the cerebral cortex and the medial temporal lobe

68
Q

The majority of CTE cases have _ __ __ __ __, with __ pathology, as intraneuronal and intraglial inclusions and neurites found in more than 80% of CTE cases

A

Tar DNA-binding protein-43
TDP-43

69
Q

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

A

true

70
Q

Neuroinflammation, as seen as __ and activated __ of the __, is a consistent feature of both __ and __

A

astrocytosis, microglia, white matter
CTE, TBI

71
Q

Where are clusters of microglia found? What is often there?

A

subcortical white matter
typically a robust astrocytosis

72
Q

__ 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)

A

amyloid-beta peptides

73
Q

__ are found in approximately 20% of CTE cases, and are found in subjects who are significantly older than those without __ __

A

alpha-synuclein-positive lewy bodies
lewy bodies

74
Q

Describe the clinical symptoms of chronic traumatic encephalopathy

A

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
Q

What are the two distinct manifestations of CTE?

A

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
Q

Advanced stage CTE is associated with __ __ and dementia is likely by stage __

A

cognitive impairment, IV

77
Q

What are potential biomarkers for CTE/ TBI?

A

cerebrospinal fluid
blood
mri
fmri
dti or dai
magnetic resonance spectroscopy
susceptibility weighted imaging
pet

78
Q

What are two potential risk factors for CTE?

A

apolipoprotein E and gender

79
Q

Apolipoprotein E in boxers and professional football players following a single TBI has been implicated in __ recovery and __ __ performance

A

prolonged, lower cognitive

80
Q

Most neuropathologically confirmed cases have been identified in __

A

men

81
Q

T/F: cognitive reserve may also play a role in the development and clinical course of CTE

A

true; cognitive reserve has been suggested as protective against clinical manifestations, argued it can confer relative resistance to neuropathological changes

Neurobiology of Adult Brain Disorders (10 decks)

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