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Neurosurgery > TBI > Flashcards

TBI Flashcards

1
Q

Definition of TBI

A

Alteration in brain function, or other evidence of pathology, caused by an external force (NINDS)
Caused by external forces, either direct impact (colliding object), non-impact (acceleration-related like in a car-crash) or penetrating injury (bullet wound)

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2
Q

Primary causes of TBI

A

traffic accidents, falls and sport-related causes

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3
Q

Prevalence of severity levels

A

light (70-95%), moderate /severe (5-30%)

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4
Q

The 3 age peaks of TBI

A

children (0-5 yr), young (15-25 yr), old (75+ yr)

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5
Q

Gender ratio of TBI

A

2:1 male:female (for children/young adults, not for elder)

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6
Q

TBI is a risk factor for?

A

Dementia & neuropsychiatric disease

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7
Q

In the sheared brain we see?

A

Microbleeding

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8
Q

In the bruised brain we see?

A

Eontusions

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9
Q

In the pressured brain we see?

A

Epidural haematomas

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10
Q

In the disconnected brain we see?

A

Progressive late white matter loss

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11
Q

What are the two mechanisms leading to heterogeneity of TBI?

A

Insult spread: it’s hard to predict where secondary damage will be worst
Focal damage
Tissue elasticity: not all tissue damages in the same way. Depending on what is damaged, the pathomechanisms will be different

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12
Q

Rodent model: controlled cortical impact (CCI)

A

Craniotomy is done and a piston is hammered on to the dura. The dura doesn’t break
Focal damage

Pros: adjust severity of injury be change pressures of pistol - it’s reproducible
Cons: long anesthesia, no immediate neural scoring, craniotomy

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13
Q

Rodent model: A penetration ballistic injury (PBLI)

A

The piston is hammered through the dura

Focal damage

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14
Q

Rodent model: cryogenic injury

A

Intact skull, exposure of skull to cold is causing focal necrosis
Focal damage

Pro: severity can be adjusted, highly reproducible and quantifiable
Cons: doesn’t mimic all we see in human TBI studies

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15
Q

Rodent model: weight-drop injury (mixed focal and diffuse)

A

A weight is falling on the skull

Pros: the most clinically relevant and closest to humans - severe can be adjusted based on drop height. It can be induced in brief anesthesia and neuro-scoring can be done shortly after lesions
Cons: high mortality due to apnea and skull fractures. One has to use many animals as the injury patterns are not reproducible

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16
Q

Rodent model: fluid percussion (FP) injury

A

Craniotomy, fluid is driven onto the exposed dura causing focal contusion and defuse neuronal injury
Mixed focal and diffuse

Pros: severity can be adjusted, it’s reproducible
Cons: requires craniotomy, which compensates for brain edema. We have high mortality

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17
Q

Rodent model: weight-drop (diffuse)

A

The weight dropping has a plate on it to level the impact out a bit

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18
Q

Rodent model: blast TBI

A

Pressure wave mimic an explosion in war

Diffuse injury

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19
Q

primary damage of TBI

A

Primary is the mechanical, immediate damage (irreversible)

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20
Q

Secondary damage of TBI

A

Secondary is the expanding injury (excitotoxicity, ion disturbances, mitochondria damage, free radicals, altered gene expression)

21
Q

Organic brain damage of TBI

A

Cause by secondary damage. Includes damage to the BBB, brain edema, increased inter-cranial pressure, inflammation, apoptosis/necrosis, ischemia, metabolic failure, axonal injury
This leads to functional deficits and brain injury

22
Q

Explain the components of excitotoxicity

A

In excitotoxicity we have increased glutamate release
Metabolic failure –> opening of voltage gated Ca2+ channels –> Increase in intracellular Ca2+ leading to excessive glutamate release. The glutamate uptake is reversed (how)?. The reversal of glutamate uptake in the astrocytes and the opening of astrocytic ion and water channels leads to astrocytic swelling and cytotoxic edema. NMDAR open –> Ca2+ in –> repeat
Cell death is caused by Ca2+ overload

23
Q

What causes excitotoxicity?

A

Energy decrease, extreme glutamate release and too much Ca2+ in the cell

24
Q

Why is it not a good idea to block NMDARs to stop excitotoxicity?

A

Synaptic NMDAR signaling can lead to neuroprotective factors

25
Q

What’s the difference between synaptic and extrasynaptic NMDAR signalling in terms of neuroprotection?

A

Enhancing synaptic activity can lead to many neuronal protection factors. Increasing extra synaptic NMDAR activity can lead to cell death

26
Q

In the study presented, what was found about NMDA signalling in mouse models of TBI?

A

TBI: after 15 min of TBI, glutamate binds more than normally, but after 8 hours it’s decreased more than normal. Decreased binding were not useful. Having NMDAR activity increased neuronal improvement and is important for functional recovery

27
Q

Is inflammation good or bad in TBI?

A

Both. Early stages of inflammation leads to clearing of debris, but later stages leads to neuronal degeneration

28
Q

M1 microglia

A

Pro-inflammatory - the ones we don’t like

29
Q

M2 microglia

A

Anti-inflammatory - the ones we like

30
Q

Microglia for severe TBI

A

is up-regulated

31
Q

Microglia in former NFL players

A

up-regulated - microglia correlated with loss of cognitive abilities

32
Q

Damage to the BB can lead to?

A

brain swelling

33
Q

How it be BBB set up?

A

Layers (from closest to the vessel to furthest away)

  1. thigh junctions created by endothelia cells
  2. Pericytes creating the basal lamina
  3. Astrocytic end-feet
34
Q

What component is responsible for the leak of the BBB after TBI?

A

Prekallikrein (in the kallikrein system).
Blocking it
1) led to less blue dye entering the brain (less leakage)
2) prevented brain swelling by measuring brain water content
3) prevented down regulation of claudin-5 protein (a tight-junction protein)

35
Q

2 types of BBB-related edema

A

cytotoxic brain edema: intracellular acidosis and ion shifts leads to cell-swelling but not brain swelling

vasogenic brain edema: Breakdown of the BBB leads to more water in the extracellular space –> leads to brain swelling, but not cell edema

36
Q

Relationship between axonal damage at tau

A

Tau usually stables axons, but during axonal damage it becomes hyper-phosphorized and aggregated into neurofibrillary tangles and neuropil threads

37
Q

What is CTE

A

Chronic Traumatic Encephalopathy (CTE)
CTE is due to multiple TBIs leading to dementia, progressive neuropsychiatric symptoms, cognitive deficits, changes in personality

38
Q

How do we diagnose CTE?

A

Diagnosis only in post-mortem neuopathology

39
Q

When was the term CTE coined?

A

1949 by Critchley to desribe “punch-drunk” better (term from 1928)

40
Q

When did Omalu first describe CTE in a NFL player?

A

In 2005

41
Q

When was the criteria and stages for CTE created?

A

2013

42
Q

Neuropathology of CTE

A 
Most important: tau 
Others:
amyloid b 
transactive response (TAR) binding protein 43 (TDP-43)
axonal degeneration
white matter degradation
neuronal loss
persistent neuroinflammation
43
Q

Stage 1 of CTE

A

headache, inability to concentrate, higher depression (no major brain atrophy)

44
Q

Stage 2 of CTE

A

increased suicidality, aggression, memory loss, mood changes (more tau on the cortical areas, also stats showing in hippocampus and amygdala, but no major cross pathology)

45
Q

Stage 3 of CTE

A

strong cognitive and executive dysfunction, depression, dementia, suicided (phosphor tau in hippocampus, amygdala, entorhinal cortex, temporal lobe). We start to see dilated vesicles

46
Q

Stage 4 of CTE

A

brain is extremely atrophied and covered with tau deposits

47
Q

CTE and microphages

A

The chronic TBI is related to immune responses (microglia remains active). Astrogliosis is also typical along with cell death and a permanent BBB dysfunction (allowing entry of the wrong microphages, which contributes to the neuronal degeneration)

48
Q

Therapy for TBI

A

None, only prevention

Neurosurgery (10 decks)

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