the injured brain Flashcards

1
Q

what is a coup/countercoup injury?`

A

damage to brain resulting from
—> initial, sudden high velocity head movement i.e. coup
followed by
—> additional injury occurring in rebound movement i.e. countercoup

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2
Q

what are the different modes of axon damage?

what are two ways in which axons respond to damage?

A
MODES OF DAMAGE:
• stretched axon
• sheared axon
• compressed axon
• twisted axon

RESPONSE TO DAMAGE:
• disturbed ion balance = increased flow of fluid and ions = axon swelling = loss of conduction = loss of function
• Wallenium degeneration = axon separates = distal end of axon degrades

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3
Q

diffuse axonal injury:

  • –> primary cause?
  • –> secondary injury?
  • –> biological changes?
A

primary cause:
• rapid tensile stretch of axons

secondary injury:
• damage to axonal cytoskeleton
• loss of elasticity
• axonal misallignment

biological changes:
• mechanical damage to sodium channels = massive sodium influx
—-> axonal swelling
—-> triggers calcium influx
—-> calcium activates proteolysis = further damage

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4
Q

what physical affects does DAI have on the brain?

A
  1. can cause haemorrhage due to axonal shearing
  2. can cause a midline shift due to axonal swelling

these affects reduce the network activity

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5
Q

epidural haemorrhage

A
  • arterial injury to the middle meningeal artery
  • normally associated with temporal bone or other skull fractures
  • has a lenticular shape
  • contained within dural sutures
  • surgical emergency
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6
Q

subdural haemorrhage

A
  • veinous injury to bridging veins
  • typically caused by cortical injury —> skull fracture may not be present
  • crescentic shape
  • not contained by dural sutures but does not cross falx cerebri or tentorium cerebelli

• often seen in elderly individuals, trauma patients, and child abuse victims
—–> brain atrophy = tension on bridging veins and increased likelihood of rupture

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7
Q

subarachnoid haemorrhage

A
  • blood in arachnoid spaces / hyperdensity in CSF
  • caused by aneurysm rupture or post-traumatic superficial cortical contusions
  • vasospasm several days after may cause secondary injruy
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8
Q

cerebral parenchymal haemorrhage

A

haemorrhage of small arterioles/capillaries in brain parenchyma

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9
Q

brain perfusion pressure (BPP) formula

A

brain perfusion pressure = mean arterial pressure - intracranial pressure

BPP = MAP - ICP

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10
Q

how is water homeostasis achieved in the brain

A

aquaporin-4 is main water channel in brain and is heavily involved in water homeostasis

AQP-4 facilitates drainage of CSF from arachnoid granulations to sinus spaces

on ventricle sides, AQP-4 used to pump water into CNS

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11
Q

what is a cytotoxic oedema?

A

swelling due to increased water intake

use an agonist of aquaporin 4 to pump out water and reduce swelling

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12
Q

what is a vasogenic oedema?

A

disruption of blood brain barrier causes water to leak into the brain

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13
Q

what is the glasgow coma scale and how does it work?

A

glasgow coma scale rates the:

1) eye opening
2) best verbal response
3) best motor response

a total GCS score is accumulated from these three categories and used to determine the severity of the injury

13-15 = mild TBI
9-12 = moderate TBI
<9 = severe TBI

the lowest GCS score is observed in the first 48 hours of the injruy

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14
Q

what are the consequences of a CNS injury to motor and sensory tracts

A

when an injury happens to sensory/motor tracts, the area not connected to the cell body can not self sustain and degrades

motor: region below lesion cannot self sustain and dies
sensory: region above lesion cannot self sustain and dies

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15
Q

what are the management and repair strategies for CNS injury?

A

MANAGEMENT:
main goal is to preserve tissue
• preservation of neural tissue (close to site of impact)
• preservation of white matter (descending/ascending pathways)

REPAIR:
• replacement of lost cells
• regrow damaged pathways
• rewire circuitry appropriately

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16
Q

difference between flaccid paralysis and spasticity

A

flaccid paralysis:
• tone of the muscles is reduced and the muscles are weak
• damage to LMN (SC to muscles)
• reflexes suppressed

spasticity:
• muscles is raised and at the same time muscles are weak
• muscles are stiff and weak
• no cortical input i.e. damage to UMN (brain to SC)
• reflexes preserved

17
Q

what are the primary and secondary injuries that result from CNS injury?

A

PRIMARY INJURY:
• mechanical i.e. force exerted onto brain/spinal cord
• immediate cell death and neural circuit disruption

SECONDARY INJURY:
• mediated by primary injury
• damaged by overexcitation
• oedema and ischemia
• inflammation ---> leads to further tissue damage/loss
18
Q

what are the SCI outcomes of trauma-induced inflammation:
• anatomical & functional correlate?
• inflammatory cell infiltrate?

A

diagram :)

19
Q

how does the complement system respond to injury?

A

BBB becomes disrupted after injury, allowing proteins to enter

proteins encounter a toxic environment of cell death and myelin debris —> activates complement system

C3 and C5 are central components of complement cascade

C5 —> MAC —> cell lysis
C3 —> C3b —> opsonisation

C3a/C5a —> engages cellular immune system = inflammatory response

20
Q

how does diffusion tensor imaging (DTI) work?

A

magnetic pulse excites tissue for numerous directions

ISOTROPIC: in CSF + spinal grey matter —> water movement in any direction

ANISOTROPIC: in white matter —> water movement restricted to along axon —> restricted by axonal membranes and myelin

fractioonal anisotropy (FA): overall degree of diffusion directionality
low FA = isotropic = grey matter =  black
high FA = anisotropic = white matter = white
21
Q

what happens to fractional anisotropy (FA) after injury?

A

normal FA for white matter = ~0.8

white matter is mostly destroyed immediately after injury

this indicates a potential therapeutic window

22
Q

what is IVIG?

A

intravenous immunoglobulin (IVIG) therapy

treatment for post-traumatic inflammation in SCI

IVIG is a liquid formulation containing purified immunoglobulin isolated from pooled blood plasma of >1,000 healthy donors

contains mostly IgG (>98%)

pushes towards “good side” of immunity i.e. repair not inflammation

already used clinically:
• antibody replacement therapy
• immunomodulatory agent in autoimmune disorders

23
Q

what is BMS scoring?

what drug is administered to improve the BMS score?

A

BMS = basso mouse scale

functional assessment of locomotor performance in mice with SCI

ranges from 0-9

0 = total paralysis
9 = normal locomotion
IVIg dose of 0.5-1g/kg is acutely administered ----> results in highest improvement in locomotion
• lesion volume reduced
• scarring reduced
• myelin increased
• reduces the decrease of FA
• reduces increase of radial diffusivity
• reduces presence of macrophages
• prevents complement activation
24
Q

what is astrogliosis?

A

astrogliosis = accumulation of reactive astrocytes at and around the lesion core

  • after CNS injury, widespread activation of astrocytes
  • reactive astrocytes accumulate at the lesion border
  • astrocytes forms wall = GLIAL SCAR
  • segregates damaged from healthy tissue —> prevents spreading of injury
  • barrier prevents axon regeneration
25
Q

what is the “balance hypothesis” ?

A

balance hypothesis:
regeneration in the adult mammalian CNS is abortive due to imbalance of growth promoting/inhibiting factors

  1. an abundance of growth-inhibitory molecules
  2. a shortage in factors that support growth
26
Q

what are the major restrictions of CNS regeneration?

A
  • limited intrinsic potential (neurons)
  • atrophy
  • absence of an ‘aligned’ (glial) substrate
  • neural scar and associated inhibitors
  • lack of sufficient trophic support (balance hypothesis)
27
Q

what is the OEG implant?

A

OEG implantation after SCI prevents secondary damage

lesion sites are reduced, but no axon regeneration