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Neurological Diseases > Module 1 > Flashcards

Module 1 Flashcards

1
Q

Classification of TBI

A 
Closed (blunt): dura remains intact
- Acceleration/deceleration
- Deformation of tissue
Open (penetrating): open dura 
- Bullets, spears etc
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2
Q

Primary TBI

A
  • Mechanical events occurring at the time of the trauma
  • Tears, lacerations, stretch, haemorrhage
  • Preventable but not amenable to pharmacological treatment
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3
Q

Secondary Injury

A
  • Delayed biochemical and physiological events
  • Oedema, NTs, ions etc
  • Accounts for much of the neurological deficit that occurs after trauma
  • The delay makes them a potential target for pharmacological intervention
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4
Q

Types of Primary TBIs

A
  • Skull fracture
  • haemorrhage (space occupying)
  • axonal injury: focal and diffuse
  • diffuse vascular injury: petechial haemorrhages
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5
Q

Primary Focal Vascular Injury (Extradural haemorrhage - haematoma)

A
  • Involves arteries
  • Form when bleeding occurs between the skull and the dura mater and the normally adherent dura is stripped from the bone
  • Space occupying lesion
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6
Q

Primary Focal Vascular Injury (Subdural haemorrhage - haemtoma)

A
  • Bridging veins are damaged and bleed
  • Space occupying lesions -> increased pressure
  • Not as quickly as extradural as veins bleed much slpwer than arteries
  • Often have a lucid interval -> onset of symptoms much slower
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7
Q

Primary Focal Vascular Injury (Subarachnoid haemorrhage)

A
  • Most common abnormality seen following head injury, usually minor
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8
Q

Primary Focal Vascular Injury (Intracerebral haemorrhage)

A
  • Are haematomas 2cm or greater in size, not in contact with the surface of the brain
  • Caused by deformation and rupture of intrinsic blood vessels
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9
Q

Primary Axonal Injury

A
  • Can be focal and diffuse
  • Axonal swelling are the histological markers of DAI
  • DAI is most common cause of vegetative state, dementia, severe disability
  • Most DAI occurs over time (secondary) therefore creating a window for therapeutic interventions
  • Can also occur as primary injury due to direct laceration of axons
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10
Q

Contusions

A
  • ‘Brian Bruises’
  • Occurs due to mechanical forces damaging small BVs and other tissue components (glia and nerve cells)
  • Damage sets in motion a cascade of events leading to haemorrhage, delayed breakdown of BBB and infarction secondary to thrombotic occlusion of BVs
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11
Q

Types of Contusions

A
  • Coup: beneath impact site
  • Contrecoup: opposite to impact site
  • Intermediate coup: middle of brain
  • Fracture contusions: occur beneath site of fracture
  • Gliding contusions: caused by movement of the brain
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12
Q

Lacerations

A
  • Disruptions of neural paranchyma occurring at moment of injury
  • Direct: penetrating injury from missiles or depressed skull fractures
  • Indirect: secondary to tissue deformation by mechanical forces (nothing actually penetrates the skull)
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13
Q

Diffuse Vascular Injury (DVI)

A
  • Numerous small haemorrhages throughout the brain
  • Common in white matter of frontal and temporal lobes
  • Very common in patients who die within minutes of a closed head injury
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14
Q

Secondary TBIs

A
  • Focal or diffuse hypoxic-ischaemic injury

- Focal or diffuse brain swelling

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15
Q

Hypoxic-Ischaemic Injury

A
  • Is likely whenever there is a reduced content of oxygen in the blood or reduced blood flow to an area in the brain
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16
Q

Diffuse brain swelling

A
  • Occurs frequently after TBI and may contribute to raising ICP
  • Occurs mainly in children and adolescents
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17
Q

Post-Traumatic Oedema

A
  • Accounts for 50% of all deaths following TBI
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18
Q

Treatment for TBI

A
  • Immediate surgery to control bleeding
  • Monitoring and controlling ICP
  • Insuring adequate BF to brain
  • currently no effective therapeutic intervention for TBI
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19
Q

Glasgow coma scale

A
  • Tests for three pateint responses: eye opening, best verbal response, best motor response
  • Scale 3 - 15
  • 3 - 8: severe head injury
  • 9 - 12: moderate head injury
  • 13 - 15: mild head injury
  • its use may be limited by confounding factors such as intoxication and ongoing medical treatment such as sedation
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20
Q

Other Assessments of TBI

A
  • In addition to GCS:
  • duration of loss of consciousness
  • post traumatic amnesia
21
Q

Concussion

A
  • Functional rather than a structural impairment
  • Two descriptions:
    1. Describes a distinct pathophysiological entitiy with its own diagnostic and management implications, mainly seen in the context of sporting injuries
    2. Describes a constellation of symptoms that arise after different types of TBI
22
Q

Diagnosis

A
  • Usually very subjective, based on self-reports, which can be overstated or concealed
  • SCAT3
23
Q

What happens to the brain following a concussion

A
  1. Mechanical injury
  2. Indiscriminate release of NTs
  3. Widespread ionic fluxes
    - Ionic environment is the same inside and outside the cell
    - > neuron can’t send any APs because there is no way to create an electric current
    - > stops the brain from being able to communicate -> loss of consciousness and amnesia
  4. Increased activity of membrane pumps to restore ionic gradient
  5. Hyperglycoloysis to generate more ATP
  6. ‘Energy crisis’: around 2-10 days afterward the brain has less glucose as the body isn’t able to keep up with the demand .: period of vulnerability
24
Q

Axonal Events Following a concussion

A
  • Neurofilament compaction
  • Microtubule disassembly and accumulation of axonally transported organelles
  • Axonal swelling
25
Q

Post-Concussion Syndrome

A
  • 5-10% of concussions will have symptoms that persist beyond 6 weeks
  • There is no known cause for these persistent symptoms
  • A prior history of concussions will increase the likelihood of PCS
26
Q

Repeated Concussion

A
  • Once a person sustains a concussion, they are 4 times more likely to sustain a second one
  • After several concussions, it requires less of a blow to cause the injury and requires longer to recover
27
Q

Long Term Effects of Repeated mTBI (concussion)

A
  • Mild cognitive impairment
  • Depression
  • Neurodegeneration: dementia, parkinson’s, ALS, CTE
28
Q

Chronic Traumatic Encephalopathy

A
  • Progressive tauopathy characterised by irregular deposition of hyperphyosphorylated (abnormal) tau
  • Unique tau deposition observed in superficial cortical layers with epicentre at the base of the sulci (this is where the mechanical forces are concentrated) and surround BVs
  • Cerebral atrophy, thinning of white matter pathways
29
Q

Tau

A
  • Microtubule associated protein
  • Helps with movement of proteins along the microtubule
  • when it is bound to the MTs it assists in stability
  • tau becomes unbound to allow the protein to move down the MT by addiding a phosphorylated tag to the tau protein
30
Q

Hyperphospharylated Tau

A
  • phosphate tags accumulate, cant be taken off the protein -> cant attach to the MTs -> MTs become unstable -> inhibition of axonal transport
  • also become sticky -> clump together -> can form neurofibrillary tangles
31
Q

Clinical Features of CTE

A
  • One of two major initial presentations:
    1. behaviour/mood variant
  • observed in younger patients (40yrs)
  • increased aggression, anxiety and depression
  • more impulsive and violent behaviours
    2. cognitive variant
  • observed in older patients
  • impaired episodic memory
  • ‘dementia like’ symptoms
32
Q

SC Structure

A
  • Cell bodies of sensory neurons located in ganglia

- cell bodies of motor neurons located in SC

33
Q

Secondary Injury

A
  • delayed and potentially reversible molecular and cellular pathophysiological mechanisms
  • these processes are characterised by neuronal cell death, astrocyte activatino, infiltration of peripheral monocytes and activation of resident microglia
34
Q

Secondary Injury: excitotoxicity

A
  • Increase in extracellular glutamate following uncontrolled release with neuronal depolarisation
  • Accumulation of intracellular calcium activates a number of calcium dependent enzymes, which degrade cellular structures and eventually cause neuronal degeneration
35
Q

Secondary Injury: oxidative stress

A
  • caused by an increased production of ROS or decreased degradation (role of antioxidants)
  • > disruption of plasma memb
  • > oxidation of proteins
  • > mutations in DNA
36
Q

Secondary Injury: Neuroinflammation

A
  • post traumatic neuroinflammatino is characterised by glial cell activation, leukocyte recruitment and upreg of inflam mediators
  • Both protective and detrimental effects for the progression of secondary brain damage have been associated with diff aspects of the immune response
37
Q

Microglia

A
  • resident immune cell in the brain
  • number of physiological functions: maintenance of tissue homeostasis, synaptic remodelling and secretion of neurotrophic factors
38
Q

Microglia following injury

A
  • Among the first responders to cns injuries

- mobilised within the hour and continue to accumulate for over a month

39
Q

Microglial activation

A
  • Resting microglia appear ramified with many short, fine processes, which allows them to sense changes in local environment
  • Activated microglia appear amoeboid, spherical, lacking processes and containing numerous phagocytic vacuoles
40
Q

Microglia activation states

A 
MI: detrimental 
- role: phagocytose and remove debris
- cytotoxicity and tissue injury 
M2: beneficial 
- role: turn off immune response and switch to tissue repair
- immune suppression and tissue repair
Ideally after insult to brain: M1 -> M2
41
Q

Microglial activation: double edged sword

A 
Exacerbate tissue damage via:
- Pro-inflam cytokines
- interferon gamma
- oxidative metabolites
- MMP-9
Also has beneficial effects: 
- phagocytose cellular debris and release anti-inflam cytokines
42
Q

Astrocyte function following insult to brain

A
  • mount a pro-inflam response: clear debris, promote tissue repair, recruit peripheral leukocytes
  • Form a barrier (glial scar) to limit spread of toxic environment created by secondary injury processes
43
Q

Neutrophils following acute brain injury

A
  • attempt to clear cell debris by phagocytosis, release growth factor for repair
  • also contributes to ongoing tissue injury following initial insult: release of ROS and MMPs -> amplify brain inflam response with more extensive activation of resident cells
44
Q

Inflammatory mediators

A
  • Cytokines, chemokines, neuropeptides
  • Regulate peripheral immune cell infiltration, microglial and astrocytic activation, apoptotic cell death, repair processes
45
Q

TNF-alpha

A
  • Pro-inflam cytokine produced by activated microglia and astrocyte
  • TNF knock out mice: do better initially but don’t recover as well later
46
Q

Chemokines

A
  • The chemotactic cytokines, or chemokines, comprise a large group of inflammatory mediators that regulate leukocyte activation and migration
47
Q

*** lecture 4 checkpoint

A

do before test!

48
Q

Persistant Inflammation

A
  • Following acute injury to the brain a subset of patients develop reactive microgliosis
  • Reactive microgliosis can be defined as a microglial activation that occurs in response to neuronal damage, which is then perpetuated by further microglial activation and neurotoxicity
  • Thus, a self-propelling and progressive cycle of microglial activation and neuron damage ensues
  • May underlie the link between acute brain injury and increased risk of neurodegenerative diseases like AD’s

Neurological Diseases (24 decks)

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