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Traumatic brain injury Flashcards

1
Q

Define Acquired brain injury

A

Injury that is not congenital, hereditary, degenerative or caused by trauma - event that occurs after birth.

There are 2 types:
1) traumatic: falls, assaults, accidents, sports injuries.
2) non-traumatic: stroke, aneurysms, tumour, infectious disease.

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2
Q

How do falls impact people of different ages differently?

A

People over 75 are 3x more likely to be hospitalised.

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3
Q

What are the different types of changes following ABI

A

1) Physical/somatic: headache, balance disturbance, motor/movement disorders, fatigue and sensory chanages.
2) Cognitive: decreased attention/concentration, poor memory, executive dysfunction, subtle language difficulties (naming and word-finding problems).
3) Emotional/behavioural: anxiety, depression, irritability, agitation, aggression.

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4
Q

What is executive function and how is it altered after brain injury?

A

Executive function:
* Thinking skills we use for:
* Problem solving
* Making decisions
* Planning and completing tasks
* Reflection
* Dysfunction symptoms:
* Loss of motivation
* Disorganised
* Loss of adaptation
* Problem solving is compromised
* Increased impulsivity
* Lack of planning

Decreased after brain injury

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5
Q

Define traumatic brain injury

A

an alteration in brain function (loss of
consciousness, post-traumatic amnesia, and
neurologic deficits) or other evidence of brain
pathology (visual, neuroradiologic, or laboratory
confirmation of damage to the brain) caused by
external force”

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6
Q

Outline link between TBI and AD

A

History of TI =2.3x more likely to develop AD.

Patients with TBI and AD have similarities. TBI is risk factor for dementia.

Also accelerates onset of cognitive impairment (true for non-dementia cases too).

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7
Q

How many people die or are hospitalised due to TBI every year?

A
  • Causes death or hospitalization of an estimated 27-69 million people each year
    (James et al., 2019)
  • Affects more than 1.7 million Americans, costing $76.5 billion
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8
Q

Link between TBI and cardiovascular disease

A

US veterans with TBI history more likely to develop cardiovascular disease.

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9
Q

Link between TBI and motor function

A

30% of TBI survivors report motor deficits.

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10
Q

Outline classification of TBI

A
  • Glasgow Coma Scale (GCS)
    measures the level of
    consciousness:
  • Mild (GCS 13-15)
  • Moderate (GCS 9-12)
  • Severe (GCS ≤ 8)
  • Reflects the risk of dying from
    TBI:
  • High (up to 40%) for severe
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11
Q

Outline the primary injury phase

A

May be:
* focal (e.g. subdural - blood collects between skull and brain surface, contusion - collection of blood outside vessel)
* Causes irreversible damage due to impairment of cells or cell death

Shockwave of brain compression and expansion causes mechanical forces in skill that damages neurons and blood vessels.

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12
Q

Diffuse injury

A

widely distributed axonal damage, vascular injury and hypoxic-ischemic.
main mechanism for diffuse is acceleration/deceleration of the head seen in car accidents.
Brain tissue is heterogenous = some parts of brain move slower than others causing sheer, tensile and compressive forces within brain tissue.
traumatic axonal injury, diffuse cerebral oedema.
Lateral head movement results in more severe damage than saggital.

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13
Q

What is TAI? give pathological hallmark

A

Traumatic axonal injury: grossly swollen axons.

Trauma evokes cascade of changes to axon which ultimately leads to secondary disconnection.

Altered focal axolemma permeabilitily, ionic homeostasis causes ca influx and mito to swell. Cytochrome c released from mito, this and ca levels results in cysteine proteins to breakdown essential axonal cytoskeleton. Anterograde transport converts to retrograde to prevent axonal swelling.
Calcineurin activated which alters microtubule network and disrupts axonal transport, organelles accumulate and there is swelling.
Andriessen et al., 2010

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14
Q

Outline focal TBI

A

Impact to head causes energy transfer to cerebral tissues and causes depolarisation.
Increase in extracellular glu = supraphysiological CA2+ influx x50 normal that initiates parallel operating intracellular cascades. (also increased Na)
Inncreased activity of ca-depdendent enzymes nNOS enhances nitric oxide production = lipid peroxidation and necrosis.
Cysteine proteases augmented and causes necrosis.
mitochondrial sequesters excess ca but as so high this ca overload leads to increased mito permeability, ROS released into the cell and apoptosis triggered.
Necrosis is ATP independent therefore occurs in tissue where mito not functioning.
Andriessen et al., 2010

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15
Q

Inflammation

A

Inflamm: BBB dys allows infiltration of neutrophils, lymphocytes in,

  • upregulation of cytokines such as tnf-alpha which acticates caspases used in cell death.

ng and lee 2019

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16
Q

Outline the subacute stage of TBI

A

Remyelination or plasticity can contribute to recovery
* This is most prominent in the 1st 3 months after injury (Fawcitt, 2009)
* GABA inhibition is important during this stage – too much is bad!
* Blocking GABAA
, but not GABAB
, improves working memory in TBI rats
(e.g. see Kobori and Dash, 2006) and motor function (e.g. see Alia et al.,
2016)

17
Q

Outline biomarkers for TBI

A

Different biomarkers were found in acute vs chronic TBI (Briana et al, 2022)
* Acute:
* Mainly metabolic and mitochondrial dysfunction (mtDNA)
* Chronic:
* Neurodegenerative processes, identified 7 days after injury
* miRNAs may be an indicator (Sandmo et al., 2022)
* TBI may be more likely to increase the risk of dementia in individuals who have a
specific variant of the gene for apolipoprotein E (APOE) called APOE-ε4:
* E.g. outcome after 6 months is worse in APOE-ε4 carriers (Zhou et al., 2008)
* 35% and 100% of TBI patients with one or two APOE ε4 alleles, respectively, possess Aβ
pathology (Nicoll et al., 1995)

  • Frailty index 0-1:
  • Significantly associated with an
    increased risk of mortality at 6
    months follow-up and severe
    disability or each 0·01 increase in
    the frailty index score, regardless of
    age (Galimberti et al., 2022)
  • GFAP ↑ with TBI
  • NfL ↑ with TBI
18
Q

What happens to interneurons in TBI?

A
  • Interneurons are extremely vulnerable to death after TBI
  • After TBI, interneurons gained more connections from neighbouring
    cells, but become disconnected from the rest of the brain
  • Interneuron transplants may help improve memory and stop seizures
    in TBI mice
19
Q

What is CTE?

A

Chronic Traumatic encephalogy: caused by repetitive impact to the head.

Found in 87% of deceased american football players

20
Q

Pharmacological treatment

A

Use of cyclosporin-A (CsA), inhibitor of MPT pore, lowered levels of
intramitochondrial Ca2+ (Sullivan et al., 1999; Kilbaugh et al., 2011)
* Methylprednisolone can inhibit TNF-α expression and NF-kB
activation (Xu et al., 1998)
* Ca2+ channel blockers such as SNX-111 (ziconotide) and (S)-emopanil
can reduce trauma-induced Ca2+ accumulation and CBF and brain
edema (Samii et al., 1999 and Hassan et al., 1999 – although latter
showed hypotensive effects in clinical trials)
* Minocycline inhibits microglial activation and release proinflammatory cytokines such as IL-6, IL-1β, and TNF-α (Homsi et al.,
2009)

21
Q

Outline non-invasive stimulation for TBI

A
  • After acute primary and secondary injuries:
  • Changes can include increased GABA-mediated inhibition during the subacute stage
    and neuroplastic alterations that are adaptive or maladaptive during the chronic
    stage.
  • tDCS and rTMS could be used:
  • Animal studies suggest that tDCS could improve motor deficit in TBI (e.g. see Li et al.,
    2015)
  • Anodal tDCS improved reaction times compared to sham controls (Kang et al., 2012)
  • Anodal tDCS could induce long-term potentiation by modulating GABAAergic and
    glutamatergic synapses (e.g. Stagg et al., 2009)
  • Cathodal tDCS could induce the long-term depression by reducing the glutamatergic
    activity (e.g. Nitsche et al., 2003)
  • More work needed!
22
Q

Outline tDCS

A

tDCS: transcranial direct current stimulation, non-invasive.

  • low intensity electric current (2 electrodes placaed over head). Alters resting mem potentials, increase or decrease depol likelihood.
  • cathode = decrease
  • anode = increase
  • applied to left DLPFC
  • side effects transient but need better targetting to determine whether correct site targetted etc.
  • Some studies showed improved coma recovery scales

Altered cognition: often memory loss etc.

  • only 1/4 of TBI improve cognition 5 yrs after.add to

Zaninotto et al, 2019h

23
Q

Outline transcranial low-level light/laser therapy (LLLT)

A

In acute phase, decrease in energy transduction
and ATP levels occur due to excessive calcium in
mitochondria -> impairing the oxidative
phosphorylation
* LLLT improve mitochondrial function, promoting
increased ATP and release of nitric oxide ->
enhances cerebral blood flow and brain oxygen
(e.g. see Rojas et al., 2008)
* 8 weeks of LED treatment led to an improvement
in attention in a patient, 7 years after initial
injury, whilst P2 showed improvements on
Stroop test (Naeser et al., 2011)

24
Q

Outline DBS

A

Deep cerebellar stimulation enhances cognitive recovery in rats
(Chan et al., 2022) -> possibly mediated by BDNF-mediated
synaptogenesis
* NAc DBS was shown in rats to improve spatial memory
performance after TBI (Aronson et al., 2022)
* 4 patients with severe TBI demonstrated functional
improvements (Rezai et al., 2016)
* Some evidence of 100Hz DBS improving functional connectivity
of whole, local and local-local brain regions in minima

25
Q

Outline stimulation of the vagus nerve

A
  • Stimulation of the vagus nerve can lead to :
  • Reduction in brain edema
  • Decrease in TNFα and interleukin-1β
  • Increase of interleukin-10 (anti-inflammatory
    cytokine) (Zhou et al., 2014)
  • Stimulate LTP in rats (Zuo et al., 2007)
  • However, in humans it can cause adverse sideeffects (George and Aston-Jones, 2010):
  • Vocal cord paresis
  • Cough
  • Dyspnea
  • Lower facial weakness

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