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PYB304 - part 2 > 10. Brain damage and neuroplasticity > Flashcards

10. Brain damage and neuroplasticity Flashcards

1
Q

What are the causes of brain damage?

A
  • brain tumours
  • cerebrovascular disorders – cell death
  • Closed-head injuries
  • infections of the brain
  • neurotoxins
  • genetic factors
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2
Q

Tumour

A

AKA neoplasm

Independently growing cell mass without any physiological function (cancer)

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3
Q

What are the types of tumours?

A
  • meningiomas
  • Infiltrating tumors
  • Metastic tumours
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4
Q

Meningiomas

A

20% of tumours; grow between meninges; encapsulated (within own membrane), usually benign

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5
Q

Infiltrating tumours

A

Most tumours are infiltrating. Grow diffusely through surrounding tissue, typically malignant, difficult to remove or destroy

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6
Q

Metastatic tumours

A

10% of brain tumours; originate elsewhere, usually lungs, skin, breasts

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7
Q

Define metastasis (NOT metastatic tumours)

A

Transmission of disease form one organ to another

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8
Q

Stroke

A

Sudden-onset cerebrovascular accident (CVA) resulting in brain damage

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9
Q

What are the types of strokes

A

Cerebro haemorrhage

Cerebral ischemia

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10
Q

Cerebral haemorrhage

A

A kind of stroke that involves bleeding in the brain. Caused by burst aneurysms (defective elasticity in artery wall).

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11
Q

How do you prevent cerebral haemorrhages?

A

By avoiding rise in blood pressure and strenuous activity

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12
Q

Cerebral ischemia

A

A kind of stroke that involves blood supply disruption caused by:

  • Thrombosis
  • Embolism
  • Arteriosclerosis
  • Sudden drop in blood pressure
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13
Q

Thrombosis

A

A former thrombus blocks artery

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14
Q

Embolism

A

Traveling thrombus lodges in narrower artery

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15
Q

Arteriosclerosis

A

Thickening of blood vessel walls

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16
Q

What are the properties of ischemia?

A

Induced in the brain
Does not develop immediately (a couple of days)
Affect some neurons more than others (e.g. hippocampus)
Different mechanisms for different brain structures
Involves brain’s own neurotransmitter

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17
Q

What does ischemia result from?

A

Results largely from excessive excitatory neurotransmitter release – especially glutamate (Excitotoxicity)
As a consequence of blockage, blood-deprived neurons become overactive and release too much glutamate
Glutamate over-activates postsynaptic glutamate receptors, esp. NMDA
Result: influx of Na+ and CA2+ into postsynaptic neurons (concentration abnormally high)
- triggers release of glutamate from postsynaptic neurons (domino effect
- Triggers internal reactions that lead to cell death (apoptosis)

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18
Q

What is the process of stroke-induced release of glutamate?

A
  1. Blood vessel becomes blocked
  2. Neurons that are affected by the ischemia release of excessive glutamate
  3. excessive glutamate binds to NMDA receptors, thus triggering an excessive influx of NA+ and CA2+ ions into postsynaptic neurons
  4. The excessive influx of Na+ and Ca2+ ions eventually kills postsynaptic neurons, but first it triggers the excessive release of glutamate from them thus spreading the toxic cascade
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19
Q

What is the sequences of damaging events with stroke?

A
  1. A blood clot stops the flow of blood to a brain region
  2. Without oxygen and glucose, neurons begin to depolarise, perhaps because of loss of the sodium-potassium pump. The neurons reach threshold and produce a barrage of action potentials
  3. Many of these rapidly firing neurons release the excitatory neurotransmitters glutamate. In addition, the lack of energy in the presynaptic neuron causes the glutamate transporters, which normally remove the transmitter from the cleft, to stop working (no reuptake)
  4. Postsynaptic neurons, bombarded with glutamate, also produce a barrage of action potentials (which may spread the glutamate flood) so excessive amounts of calcium and zinc enter the cell
  5. The excessive intracellular calcium and zinc trigger cell death (apoptosis), and the neuron has succumbed to excitotoxicity.
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20
Q

What are the possible treatments for strokes?

A

Thrombolytics and drugs

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21
Q

Thrombolutics as a treatment for strokes

A

Thrombolytics are drugs that dissolve blood clots. Includes tissue plasminogen activator, may restore blood flow to avoid further amage

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22
Q

What are the types of drugs that treat stroke?

A
  • drugs that inhibit the voltage-gated sodium channel may reduce the number of action potentials generated
  • Drugs that block glutamate receptors may combat the excessive stimulation
  • Drugs that block calcium channels may avert the intracellular buildup of calcium
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23
Q

What are the kinds of cell death?

A

Apoptosis and necrosis

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24
Q

Apoptosis

A

Active but gradual self-destructive process
Important adaptive process in limiting brain damage
Important in development: culling excess neurons

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25
Q

How does Apoptosis limit brain damage?

A

Cell body shrinks and remainder of neuron dies, any debris is cleared (vesicles) and thus there is no trauma to surrounding cells

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26
Q

Necrosis

A

Passive and fast but more generally destructive process
Neuron swells and breaks up (axons and dendrites, followed by cell body)
Fragmentation may cause inflammation and damage cells in surrounding tissues

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27
Q

Close-head injuries

A

Brain injuries due to blow that do not penetrate the skull – the brain collides with the skull

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28
Q

What are types of close head injuries?

A

Contrecoup injuries

Concussion

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29
Q

Contrecoup injuries

A

Contusions are often on side of brain opposite to the blow. e.g. the blow was made at the front but the impact actually occurred at the back.

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30
Q

Contusions

A

Damage to cerebral circulatory system, resulting in internal bleeding and a haematoma

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31
Q

Haematoma

A

Bruise/clotted blood

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32
Q

Concussion

A

Disturbance of consciousness but no evidence of structural damage (e.g. contusion).
Nothing to worry about??? – Punch-drunk syndrome

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33
Q

Punch-drunk syndrome

A

Dementia pugilistic and cerebral scarring

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34
Q

What are brain infections caused by?

A

Invasion by microorganisms → encephalitis – the resulting inflammation

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35
Q

What are the types of brain infections?

A
  1. bacterial infections

2. viral infections

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36
Q

Bacterial infections

A

Often leads to cerebral abscesses (pockets of pus)
May inflame meninges → meningitis
Syphilis

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37
Q

Syphilis

A

Transmitted via genital sores and can result in general paresis (syndrome consisting of insanity and demetia)

38
Q

Viral infections

A

Some viral infections preferentially attack neural tissue (e.g. rabies) – virus typically dormant for one month

39
Q

Neurotoxins

A 
May enter general circulation from gastrointestila tract, lungs, or through the skin.
These can be endogenous (think glutamate)
Recreational drugs (e.g. alcogol, ecstacy) may cause brain damage – neurotoxic effects of alcohol and thiamine deficiency
40
Q

Toxic psychosis

A

Chronic insanity produced by neurotoxins (e.g. mercury, lead)
Some antipsychotic drugs have toxic effects and produce a motor disorder – tardive dyskinesia

41
Q

How do genetics play a factor in neuropsychological disease?

A

Most neuropsychological disease of genetic origin are associated with recessive genes

42
Q

What is an example of genetic factors affecting neuropsychological diseases?

A

Down syndrome

  • genetic accident – not faulty gene
  • 0.15% of births, probability increases with advancing maternal age
  • Extra chromosome 21
  • Characteristic disfigurement, mental retardation, other health problems
43
Q

What are some neuropsychological diseases?

A

Epilepsy
Parkinson’s disease
Alzheimer’s disease

44
Q

Epilepsy

A

Primary symptom is seizures
Difficult to diagnose – epileptic seizures are diverse and complex
No single cause

45
Q

How are seizures generated?

A

By chronic brain dysfunction

46
Q

What are the results of epilepsy?

A

Convulsions – motor seizures

Subtle changes of thought, mood or behaviour

47
Q

What are the potential causes of epilepsy?

A 
Brain damage (many and varied)
Genes → 70 known so far
48
Q

How is epilepsy diagnosed?

A

EEG – Electroencephalogram

Seizures associated with high amplitude spikes

49
Q

What are the two major groups of seizures?

A

Partial seizures and generalised seizures

50
Q

What are the two kinds of partial seizures?

A

Simple partial and complex partial

51
Q

Simple partial seizures

A

Symptoms are primarily sensory or motor or both (Jacksonian seizures)
Symptoms spread as epileptic discharge spreads
No loss of awareness

52
Q

Complex partial seizures

A

Often restricted to the temporal lobes (temporal love epilepsy)

  • patient engages in compulsive and repetitive simple behaviours – automatisms
  • more complex, seemingly normal behaviours also occur
53
Q

What are the two kinds of generalised seizures?

A

Grand mal and Petit mal

54
Q

Grand mal

A

Loss of consciousness and equilibrium
Tonic-clonic convulsions – rigidity (tonus) and tremors (conus)
Resulting hypoxia may cause brain damage

55
Q

Petit mal

A

Not associated with convulsions
Disruptions of consciousness associated with a cessation of ongoing behaviour (petit mal absence)
Different EEG pattern (bilaterally symmetrical 3-per-second spike-and-wave discharge)

56
Q

What is the kindling model of epilepsy?

A

A series of periodic brain simulations eventually elicits convulsions – kindling phenomenon (Goddard et al., 1969)

  • Neueoplastic changes are permanent
  • produced by stimulation disturbed over time
57
Q

Why is the kindling model of epilepsy a model of interest?

A

Because it is elicited it is not spontaneous

  1. Convulsions are similar to those seek in some forms of human epilepsy – but they only occur spontaneously if kindled for a very long time
  2. Kindling phemenon is comparable to the development of epilepsy (epileptogenesis) seen following a head injury
58
Q

Parkinson’s disease

A

Progressive motor disorder
Pain and depression common before full disorder develops
Cognitive deficits emerge by dementia is not typically seen?

59
Q

What the common symptoms of Parkinson’s Disease?

A

Tremor at rest

60
Q

What are the causes of Parkinson’s disease?

A

No single clause
Associated with degeneration of the substantia nigra (dopaminergic neurons)
Almost no dopamine in the substantia nigra and straitum of Parkinson’s patients

61
Q

How is Parkinson’s Disease treated?

A

Temporarily with L-dopa

62
Q

What is Parkinson’s Disease linked to?

A

Linked to 10 different gene mutations (affect mitochondria function)

63
Q

What is the MPTP model of Parkinson’s Disease?

A

The case of Frozen Addicts (Lanston, 1985)

  • Synthetic heroin produces the symptoms of Parkinson’s
  • contained MPTP (neurotoxins)
64
Q

What does MPTP cause?

A

Causes cell loss in the substantia nigra (like that seen in PD) → loss of dopaminergic cells leads to decline in dopamine

65
Q

What does MPTP cause?

What did animals studies of the MPTP model find?

A

Animal studies led to the finding that deprenyl can slow down the progression of PD

66
Q

Deprenyl

A

Is a monoamine agonist – blocks the effect of MPTP (slow down development)

67
Q

Alzheimer’s Disease

A 
Most common (but not only) cause of dementia – likelihood of developing it increases with age.
Pattern diffuse but more concentrated in medial temporal lobe structures (entohinal cortex, amygdala, hippocampus)
68
Q

How is Alzheimer’s disease progressive?

A

Early stage: confusion and selective decline in memory
Intermediate stages: confusion anxiety, speech problems
Final stage: loss of control of functions

69
Q

How is Alzheimer’s disease diagnosed?

A

Definitive diagnosis only at autopsy

  • neurofibrillary tangles
  • amyloid plaques (scar tissue)
  • neuronal loss
70
Q

What was the transgenic mice and Alzheumer’s disease study?

A

Transgenic – genes of another species have been introduced
Only humans and a few related primates develop emyloid plaques.
Genes accelerating human amyloid synthesis introduced into mouse eggs and implanted
- plaque distribution in transgenic mice comparable to that in AD, and associated memory problems observed
- No neurofibrillary tangles

71
Q

What are the neuroplastic responses to damage?

A
  1. Neural degeneration – deterioration
  2. Neural regeneration – re-growth of damaged neurons
  3. Neural reorganisation
  4. Recovery of brain function
72
Q

Types of Neural degeneration

A

Axtomoy
Anterograde
Retrograde
Transneuronal degeneration

73
Q

Axtomoy of neural degeneration

A

Cutting axons
Method to study responses to neuronal damage
Cutting a neuron’s axon results in two forms of neural degeneration
- anterograde degeneration
- Retrograde degeneration

74
Q

Anterograde neural degeneration

A

Distal portion of neuron degenerates quickly

75
Q

Retrograde Neural degeneration

A

Proximate portion of the neuron may degenerate o regenerate slowly (depending on reaction of cell body)

76
Q

Transneuronal degeneration neural degeneration

A

Degeneration transmitted from damaged neurons to intact neurons via synaptic connections

77
Q

Neural regeneration

A

Not successful in mammals and other higher vertebrates – capacity for accurate axonal growth is lost in maturity
Regeneration is virtually non-existent in the CNS of adult mammals and unlikely, but possible, in the PNS

78
Q

How does regeneration in the PNS start?

A

Re-growth starts 2-3 days after injury.

79
Q

How does regeneration occur when the schwann cells myelin sheath is intact?

A

Regeneration axons may grow through them to their original targets (mm per day).

80
Q

How does regeneration occur when the nerve Is severed and the ends are separated?

A

They may grow into incorrect sheaths toward incorrect destinations

81
Q

How does regeneration occur when the ends of the neurons are widely separated?

A

No meaningful regeneration will occur

82
Q

Why do mammalian CNS neurons regenerate in the PNS?

A

CNS neurons can regenerate if transplanted into the PNS, while PNS neurons will not regenerate in the CNS → PNS environment

83
Q

How do Schwann cells (PNS) promote regeneration?

A

Schwann cells (PNS) promote regeneration through

  • neurotrophic factors – stimulate new axon growth
  • CAMs (Cell Adhesion Molecules) – provide a pathway
84
Q

How do oligodendroglia (CNS) promote regeneration?

A

Oliodendroglia release substances actively blocking regeneration

85
Q

Neural reorganisation?

A

Reorganisation of the primary sensory and motor systems has been observed following damage to:

  • peripheral nerves
  • primary cortical areas
86
Q

What is the animal example of neural reorganisation?

A

Lesion one retina and removal of other – V1 neurons that originally respond to lesioned area now responded to an adjacent area – remapping occurred within minutes

87
Q

What is the human example of neural reorganisation?

A

Imaging studies with blind patients – auditory and somatosensory cortex is comparatively larger (Elbert er al., 2002) – superior performance on relevant tasks compared to sighted individuals (Gougoux et al., 2005)

88
Q

How/why does damage lead to reorganisation?

A

Two possible mechanisms:

  1. Strengthened existing connections (release from inhibition?) – consistent with speed and localised nature of recognition)
  2. establishment of new connections – Collateral sprouting – magnitude can be too great to be explained by changes in existing connections
89
Q

What is the two-stage model of neural reorganisation?

A
  1. Release from inhibition strengthens existing connections

2. Collateral sprouting results in new connections

90
Q

How does recovery occur of CNS function?

A

Poor understood
Almost non-existent
Difficult to differentiate between compensation and true recovery (e.g. improvements due to reduction in brain swelling after injury)
Role of cognitive reserve?
Neurotransplantation (implantation of embryonic tissue/stem cells/injection of targeted versus/growth factors
Rehabilitative training

PYB304 - part 2 (6 decks)

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