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NAS > L22 - Damage and repair in the CNS > Flashcards

L22 - Damage and repair in the CNS Flashcards

1
Q

Why is repair in the injured CNS so complicated?

A
  • Complexity from cell to tissue at the expense of individual mortality
  • Complexity from mulitpotent cell to neuronal networks at the expense of reparability
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2
Q

What does the severity of injury depend on?

A

Depends on site and size - not type of injury

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3
Q

What is the energy supply of the brain like?

A
  • Consumes 15% of the energy generated in the body
  • No energy stores of its own (small amount of glycogen in astrocytes)
  • Energy is derived exclusively from glc metabolism
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4
Q

What are the 4 major types of skull fractures?

A
  1. Linear (most common) - break in a cranial bone resembling a thin line, without splintering, depression or distortion of bone
  2. Depressed - usually resulting from blunt force trauma; broken bones displace inwards
  3. Diastatic - widens the sutures of the skull and usually affects children under 3
  4. Basilar - break of bone in base of skull
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5
Q

What is hypertensive cerebral haemorrhage?

A

Hypertension causing arteries to rupture, therefore releasing blood into the brain tissue (type of stroke) –> lead to possible dec O2 supply to brain if compression of bleed is high

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6
Q

What is lobar haemorrhage?

A

Occurs when there is bleeding into a lobe of the cerebrum

- A subtype of intracranial haemorrhage

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7
Q

What is cerebral amyloid angiopathy?

A
  • A condition in which amyloid proteins build up on the walls of the arteries in the brain
  • Inc the risk for stroke caused by bleeding and dementia
  • Accumulation of amyloid proteins in cerebral vessels
  • Mutations in the APP gene are most common cause
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8
Q

What are arterio-venous malformations?

A
  • A tangle of abnormal and poorly formed BV (arteries and veins)
  • Arteries in brain cannot directly connect to nearby veins without having capillaries between them
  • Higher rate of bleeding than normal
  • Extreme press on walls of affected BV, causing them to be thin or weak
  • Can rupture due to pressure and dmg to BV
  • Can occur anywhere in the body
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9
Q

What are aneurysms?

A
  • Enlargement of an artery caused by weakness in the arterial wall –> leading to bulge, distension of artery
  • Often no symptoms
  • Ruptured brain artery can be fatal –> subarachnoid haemorrhage –> can cause extensive brain dmg
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10
Q

What are lacunar infarcts?

A
  • Small noncortical infarcts (a small localised area of dead tissue resulting from failure of blood supply) caused by occlusion (the blockage or closing of a BV) of a single penetrating branch of a large cerebral artery (smaller arteries supplying deep brain structures)
  • Type of ischaemic stroke
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11
Q

What are the possible consequences of traumatic brain injury?

A
  1. Haematomas (epidural and subdural) - compression of the brain –> raises intracranial pressure
  2. Contusions and diffuse axonal injury
  3. Hypoxic injury –> focal ischaemic lesins
  4. Multiple lesions and different types of lesions
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12
Q

What happens in an energy crisis in the brain (? causes)?

A
  • Drop in cerebral perfusion (global ischaemia) - cardiac arrest of severe hypotension (Shock)
  • Hypoxia –> CO poisoning
  • Hypoglycaemia
  • Severe anaemia
  • Generalised seizures
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13
Q

Which functions would be affected if the cervical nerves were damaged?

A
  • Head and neck
  • Diaphragm
  • Wrist extenders
  • Triceps and hand
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14
Q

Which functions would be affected if the thoracic nerves were damaged?

A
  • Chest muscles

- Abdominal muscles

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15
Q

Which functions would be damaged if the lumbar nerves were damaged?

A
  • Leg muscles
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16
Q

Which functions would be damaged if the sacral nerves were damaged?

A
  • Bowel

- Bladder

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17
Q

What are the different types of haemorrhages?

A
  1. Epidural haemorrhage
  2. Subdural haemorrhage
  3. Subarachnoid haemorrhage
  4. Intracerebral haemorrhage
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18
Q

How could traumatic brain injuries occur?

A
  1. Impact - cerebral contusions and lacerations

2. Movement of the brain inside the skull - subdural haematoma and diffuse axonal injury

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19
Q

What is an epidural haemorrhage?

A
  • Bleeding between dura mater and skull (calvarium)
  • Biconvex shape (lemon shape)
  • Limited by cranial structures, but not by venous sinuses
20
Q

What is a subdural haemorrhage?

A
  • Bleeding in subdural space; potential space between the dura and arachnoid mater
  • Concave shape (crescent/ banana)
  • Occurs more freq in elder patients due to reduced brain volume and stretched bridging veins
21
Q

What is a subarachnoid haemorrhage?

A

Bleeding within the subarachnoid space

22
Q

What is an intracerebral haemorrhage?

A

Bleeding within the brain tissue itself

- Stroke can occur from ischaemia

23
Q

Typical cause of epidural haemorrhage?

A
  • Assoc with history of head trauma and freq assoc with skull fracture
  • Typically from torn middle meningeal artery
  • Assoc with lucid interval (patient conscious and appears normal), as blood acc, headache will wrosen and mental status decline as intracranial press inc
24
Q

Typical cause of subdural haemorrhage?

A
  • Mainly due to head trauma
  • Can happen to any age group
  • Stretching and tearing of bridging cortical veins as they cross the subdural space to drain into an adjacent dural sinus
  • These veins rupture due to forces when sudden change in velocity of head
25
Q

Typical cause of subarachnoid haemorrhage?

A
  • Ruptured aneurysm
  • Head trauma
  • AVM
26
Q

Typical cause of intracerebral haemorrhage?

A
  • Hypertension
  • Head trauma
  • Arteriovenous malformation
27
Q

How could traumatic brain injuries occur?

A
  1. Impact - cerebral contusions and lacerations

2. Movement of the brain inside the skull - subdural haematoma and diffuse axonal injury

28
Q

Can epidural haematomas cross suture lines and why?

A

Does not cross suture lines because of tight adherence of dura to calvarium (therefore resulting in biconvex shape)

29
Q

Can subdural haematomas cross suture lines and why?

A

Can cross suture lines since bleeding is below the dura, which is tightly attahed to the calvarium (therefore leading to crescent shape)

30
Q

What is pseudolaminar necrosis? (cortical laminar necrosis)

A

Necrosis of neurones in brain cortex in situations when O2 supply and glc is inadequate to meet regional demands

  • Consequence of neurones being more metabolically active than glial cells or adjacent white matter
  • Selective vulnerability of certain of different neuronal popns
31
Q

What is a possible reason for the selective vulnerability in laminar necrosis?

A

Selective vulnerability of grey matter may be due to higher met demands and denser conc of receptors for excitatory aa that are released after an anoxic-ischaemic even

32
Q

What is an anoxic brain injury?

A
  • Not usually caused by blow to head

- Occurs when brain is deprived of oxygen –> if for too long, neural cells begin to die by apoptosis

33
Q

What are some possible consequences to TBI?

A
  1. Neuronal death and tissue loss
  2. BBB breakdown and oedema
  3. Gliosis and cell infiltration
  4. Upregulation of inflammatory mediators
34
Q

What are the progressive changes you can see in a cerebral infarct?

A
  1. 1 - 2 days tissue swelling –> anoxic neurones
  2. 2 weeks tissue necrosis –> neovascularisation (formation and remodeling of vessels - a response observed after injury)
  3. 2 months –> glial scar
35
Q

What are the consequences of CNS injury?

A
  1. Loss of cells and connections
    - Functional deficit
    - BBB breach
  2. Response to injury
    - Inflammatory response
    - Oedema
    - Gliosis (nonspecific reactive change of glial cells; prolif or hypertrophy of several diff types of glial cells)
  3. Long term consequences
    - Sequela (future condition caused by this injury)
    - Repair?
36
Q

What are the long term consequences of severe TBI?

A
  • Seizures
  • Focal neurologic deficits
  • Dementia
  • Persistent vegetative state
  • Inc risk of Alzheimer’s disease
37
Q

Briefly explain the repair and regen of damaged neurones

A

PNS: Axonal regen present
- Macrophage clears debris after injury
- No inhib molcs present; extending growth core
CNS: No axonal regen
- No macrophage to clear debris after axonal injury
- Inhib molcs present
- BUT CNS NEURONES DO HAVE INTRINSIC CAPACITY TO REGEN - rehab is possible

38
Q

What are some of the treatment options for CNS injury?

A
  1. Surgery
    - Remove haematoma
    - Repair skull fractures
    - Decompression
  2. Medication
    - Anti-seizure med to red reisk
    - Red oedema with diuretics
    - Induced coma to red O2 and nutrient requirements
  3. Rehabilitation
39
Q

What is neurorehab?

A

A process whereby patients who suffer from impairment following neurological diseases regain their former abilities, or if full recov not poss, achieve their optimum physical, mental, social and vocational capacity

40
Q

Describe the inhibitory environment found in CNS injury

A
  • Lack of neurotrophic stimulation
  • Neuronal death
  • Demyeliantion
  • Glial scar
  • Inhibitory molcs (Assoc with glial scar and damaged myelin)
  • Reactive astrocytes up-reg inhib extracellular matrix (ECM) molcs that inhibit regen
41
Q

What is neurological recovery?

A

Early recov –> local processes

Late recov –> neuroplasticity; modification in structural and functional organisation

42
Q

What is functional recovery?

A
  • Recovery in everyday function with adaptation and training in presence/ absence of natural neurologic recovery
  • Dependent on quality, intensity of therapy and patent’s motivation
43
Q

What are the neuronal plasticity signalling mechanisms involved?

A

Neuronal activity –> neurotrophin synthesis –> neurotrophin secretion –> neurotrophin signalling –> postsynaptic responsiveness OR synaptic morphology OR presynaptic NT release OR memb excitability –> mod of synaptic transmission and connectivity

44
Q

What are the neuroplasticity principles?

A
  1. Use it or lose it
  2. Use it and improve
  3. Specificity
  4. Repetition
  5. Intensity
  6. Time
  7. Salience
  8. Age
  9. Interference
45
Q

What is functional plasticity of the brain?

A

Brain’s ability to move functions from a damaged area to other undamaged areas

46
Q

What is structural plasticity of the brain?

A

Brain’s ability to change physical structure as a result of learning

47
Q

What are some experimental strategies for treatment of CNS injury?

A
  1. Trophic support
    - Neurotrophic factors to neuronal cell bodies
  2. Inhibiting the inhibitors
  3. Endogenous stem cells
    - Neurogenesis
  4. Cell therapy
    - Replace dead cells
    - Create favourable enviro
    - Bridge cyst cavities
    - Autologous stem cells

NAS (12 decks)

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