Wk11 Damage And Repair In The CNS Flashcards

1
Q

Head injury facts

A
  • in 2013-14 there were 162,544 admissions for head injury
  • admissions in uk with brain injury related diagnosis increased by 10% since 2005-6
  • men are 1.6x more likely than females to be admitted for head injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is repair in the Injured CNS so complicated?

Cell to tissue

A
Proliferation and migration
Contact inhibition of proliferation 
Loss of neighbouring cells
Réactivation of neighbouring cells
Réactivation of proliferation
Tissue repair (damage accumulates)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

From multipotent cell to neuronal networks

A

Proliferation and migration
Neuronal differentiation —> synapse formation
Synapse plasticity —> altered connectivity and network reorganisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

C1 to C8 functions affected

A
Cervical nerves
Head and neck
Diaphragm
Wrist extenders
Triceps and hand
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T1 to t12 functions affected

A

Thoracic nerves
Chest muscles
Abdominal muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

L1 to L5 functions affected

A

Lumbar nerves

Leg muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

S1 to S5 functions affected

A

Sacral nerves
Bowel
Bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what do functional consequences of injury rely on?

A

Depend on the site and size of the injury not the type of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Energy supply - brain

A

– 2% of the total body mass
– 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 glucose metabolism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cerebral amyloid angiopathy and lobar hemorrhage

A

Alzheimer’s

Fibrous protein deposits become brittle leading to giant haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Arterio-venous malformations

A

Large number of dilated blood vessels with bad walls - can form embolisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Aneurisms

A

Blood coagulated over time - increased inter cranial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lacunar infarcts and white matter damage

A

Tissue dies and leads to liquid filled hole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Traumatic brain injury

A
  • Impact - cerebral contusions and lacerations
  • Movement of the brain inside the skull - subdural hematoma and diffuse axonal injury

Consequences:
• Hematomas (epidural and subdural ) – compression of the brain, raised intracranial pressure
• Contusions and diffuse axonal injury - structural brain damage
• Hypoxic injury, focal ischemic lesions
• Multiple lesions and different types of lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hypoxia - ischemic brain injury

A
– Drop in cerebral perfusion (Global ischemia) - cardiac arrest or severe hypotension (shock)
– Hypoxia - CO poisoning
– Hypoglycemia
– severe anemia
– generalized seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Anoxic neurons

A

Differential sensitivity of different neuronal populations:
– Ischemia lasting 4-5 minutes – irreversible damage:
• hippocampal and neocortical pyramidal cells
• striatal neurons
• Purkinje cells
– More protracted ischemia – irreversible damage:
• thalamic and brainstem neurons

17
Q

Pseudolaminar and laminar necrosis

A

Selective vulnerability of different neuronal populations

18
Q

The progressive changes following a cerebral infarct

A

1-2 days tissue swelling Anoxic neurones
2 weeks tissue necrosis neovascularisation
2 months – glial scar

19
Q

Consequence of CNS injury

A
• Loss of cells and connections 
– Functional deficit
– BBB breach
• Response to injury
– Inflammatory response 
– Oedema
– Gliosis
• Long term consequences
20
Q

Traumatic brain injury

A
Long term consequences of severe TBI:
– Seizures
– Focal neurologic deficits
– Dementia
– Persistent vegetative state
– Increased risk of Alzheimer's disease.
21
Q

Features of CNS injury

A

CNS axons intrinsic capacity for regeneration

Inhibitory environment

  • lack of neurotrophic stimulation
  • neuronal death
  • demyelination
  • glial scar
  • inhibitory molecules: associated with glial scar proteoglycans and associated with damaged mussel in Nogo, MAG, OMgp
22
Q

Treatment options for CNS injury

A
• Surgery
– remove a hematoma 
– repair skull fractures 
– decompression
• Medication
– Anti-seizure medication 
– reduce risk for seizures
– Reduce oedema 
– diuretics
– Induced coma 
- reduce oxygen and nutrient requirements
• Rehabilitation
23
Q

Types of recovery

A

• Neurological recovery
– Early recovery (Local Processes)
– Late recovery (Neuroplasticity) modification in structural and functional organization
• Functional recovery
– Recovery in everyday function with adaptation and training in presence/ absence of natural neurologic recovery
– Dependent on quality ,intensity of therapy & patient’s motivation

24
Q

Neuroplasticity Principles

A
  1. Use It or Lose It
  2. Use It and Improve
  3. Specificity
  4. Repetition Matters
  5. Intensity Matters
  6. Time Matters
  7. Salience Matters
  8. Age Matters
  9. Interference
25
CNS injury prognosis
* Most improvements in ADLs occurs during the 1st 6 months * Up to 5% of patients may show improvement even at 12 months post- stroke * Recovery could take 2 years or more * Prognosis in patients with mild or moderate stroke is usually excellent
26
Experimental strategies for treatment of CNS injury
``` • Trophic support – Neurotrophic factors to neuronal cell bodies • Inhibiting the inhibitors – NOGO antibodies – Digestion of GSPG – Chondroitinase – Rho inhibitors (siRNA) • Endogenous stem cells – Neurogenesis – subventricular zone, subgranular ```