Damage and Repair in the CNS Flashcards Preview

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Flashcards in Damage and Repair in the CNS Deck (20)
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1
Q

Why is repair in the CNS less feasible than in the PNS?

A

The complexity of the CNS is at the expense of repairability.

2
Q

As a general rule, what functions will be affected after injury to a particular segment of the CNS?

A

Movement, sensation and autonomic control below the level of the injured segment will be affected.

3
Q

What do the functional consequences of CNS injury depend on?

A

The site and size of the injury only.

-Not the type of injury.

4
Q

Where is the energy consumed by the brain derived from?

A

Glucose metabolism; the brain has no energy stores of its own other than glycogen in astrocytes (small).

5
Q

What is the difference between a depression fracture and a compound fracture?

A
  • A depression fracture is a break in cranial bone causing depression of the bone towards the brain.
  • A compound fracture is a piercing or splintering of cranial bone.
6
Q

What is a haematoma?

A

Compression of the brain due to raised intracranial pressure.

7
Q

What is a contusion?

A

A region of injured tissue or skin in which blood capillaries have been ruptured; a bruise.

8
Q

What is traumatic brain injury?

A
  • Movement of the brain inside the skull due to impact.

- Causing cerebral contusions, lacerations and subdural haematomas.

9
Q

Which cells of the brain will experience irreversible damage after ischaemia lasting 4-5 minutes?

A
  • Hippocampal cells
  • Pyramidal cells
  • Striatal neurones
  • Purkinje cells
10
Q

Which cells of the brain will experience irreversible damage after ischaemia lasting more than 4-5 minutes?

A

Thalamic and brainstem neurones.

11
Q

What does anoxic mean?

A

Without oxygen.

12
Q

What is oedema?

A

A condition where an excess of watery fluid collects in the cavities or tissues of the body.

13
Q

Why might an oedema occur after a traumatic brain injury?

A

As a result of an inflammatory response to an injury.

14
Q

List 5 consequences of severe traumatic brain injury.

A

– Seizures.

– Focal neurologic deficits.

– Dementia.

– Persistent vegetative state.

– Increased risk of Alzheimer’s disease.

15
Q

Why is there no axonal regeneration in the CNS?

A

• Due to the presence of inhibitory molecules such as:

  • Nogo
  • MAG
  • OGmp
  • CSPG
  • Due to the lack of neurotrophic stimulation.
  • Due to the formation of glial scars.
  • Due to the demyelination of axons.
16
Q

What do glial scars consist of?

A

Primarily astrocytes and proteoglycans.

17
Q

What are the treatment options for CNS injury?

A

• Surgery:
– remove a hematoma
– repair skull fractures
– decompression

• Medication:
– Anti-seizure medication
– Reduce oedema using diuretics
– Induced coma - reduce oxygen and nutrient
requirements

• Rehabilitation

18
Q

What is neuroplasticity?

A

The brain’s ability to reorganise itself by forming new neural connections.

19
Q

Describe the mechanisms involved in neuroplasticity.

A

• Neuronal activity stimulates neurotrophin synthesis and secretion, causing:

  • Change in postsynaptic responsiveness.
  • Change in synaptic morphology.
  • Change in presynaptic transmitter release.
  • Change in membrane excitability.

•Contributes to the modification of synaptic transmission and connectivity.

20
Q

In the injured CNS environment, which ells up-regulate the inhibitory extracelluar matrix?

A

Astrocytes.