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B and Neuro > Degeneration of Nervous system > Flashcards

Degeneration of Nervous system Flashcards

1
Q

Neurodegeneration

A

‘Progressive damage or death of neurons leading to a gradual deterioration of the bodily functions controlled by the affected part of the nervous system.’

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2
Q

Acute neurodegeneration

A

Stroke

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3
Q

Chronic neurodegeneration

A

Alzheimers, Parkinsons, Huntington’s Chorea

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4
Q

Cerebral stroke

A

Blockage/interruption of cerebral artery

Death of cells

Symptoms – depend on location

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5
Q

Prevalence of strokes

A
  • In the UK
    250-400 strokes per 100 000 people

3rd cause of death

1st cause of disability (in adults)

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6
Q

Ischemic stroke (80%)

A

Occur when blockage within blood vessel - stops flow or reduces flow to area of the brain

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7
Q

Haemorrhagic (20%)

A

Individual experiences area of bleeding as blood vessel bursts

High blood pressure

Cerebral arteries under pressure

Haemorrhagic stroke

May experience anuerism

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8
Q

Risk of stroke

A

At all stages of lifespan
Important factor but can occur at any stage
1 in 4 working age adults

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9
Q

Risk Factors

A

Age
Medical conditions (high blood pressure, diabetes, high cholesterol etc.)
Lifestyle (smoking, drinking, diet, exercise)
Family history and ethnicity (Likely related to incidence of other risk factors (e.g diabetes, high cholesterol)
Specific for women (pregnancy, contraceptive pill)

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10
Q

Clinical symptoms

A

symptoms depend on where the stroke is occurring

Sudden or gradual onset
One sided limb weakness/paralysis
Confusion, loss of speech or vision
Headache
Loss of consciousness

= results in dysfunctional cognitive and motor behaviour… determined by size and location of cell loss

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11
Q

Cognitive impairment

A

Amnesia
Inattention
Confusion
Depression
Mood and behavioural changes

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12
Q

Depression

A

Common after stroke

Often differ from those with primary depression, they have more cognitive impairment, irritability, more psychomotor slowing and more mood liability

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13
Q

Transient Ischemic Attach (TIA)

A

Transient episode of neurological dysfunction without acute tissue death
- Disruption of CBF
- Mini-strokes
- Risk factor for subsequent stroke
* 10% strokes within 90 days of TIA
- Silent strokes
* No visible symptoms

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14
Q

Cerebral Stroke pathology

A

Massive cell death - caused by excessive amounts of glutamate

Inflammation, cell death, reperfusion - trying to re-establish blood flow

Inflammation

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15
Q

Inflammation

A
  • Sodium ions – water, swell, inflammation

Microglia – become phagocytic
Phagocytosis = ‘cell-eating’

Blood-brain barrier breakdown – influx of blood-borne immune cells (neutrophils, macrophages)

Oedema formation, adhesion molecules, cytokines (brain swelling, stroke0

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16
Q

Mechanisms of cell death

A

Necrosis and Apoptosis

17
Q

Necrosis

A

decrease in oxygen

depleted ATP

Cellular swelling and membrane break down

18
Q

Apoptosis

A

= triggering of the death programme

Intracellular signalling

Cells fragment into vesicles

Phagocytosis

19
Q

Hyperperfusion

A

A major increase in CBF, well above metabolic demands of the CNS tissue

20
Q

Intracranial haemorrhage/edema

A

Mortality 36-63%
80% patients significant morbidity

21
Q

Excitatory neurotransmitters

A

glutamate and aspartate

22
Q

Inhibitory neurotransmitters

A

GABA and glycine

23
Q

Closely related neurotransmitters

A

GABA and Glutamate

24
Q

Lucas and Newhouse 1957

A

glutamate caused retinal damage

25
Q

Olney 1969

A

glutamate produced brain damage in neonatal mice

26
Q

Ultrastructural studies

A

amino acid treatment = postsynaptic (but not presynaptic) alterations

Excitotoxic hypothesis

Excess amino acids results in prolonged depolarization of receptive neurones which in some way* leads to their eventual damage or death

27
Q

GABA system

A

functions in opposite to glutamate

during ischemia - GABA accumulates in extracellular space

Increase activation in GABA override excessive excitation of glutamate

28
Q

Stroke treatments

A

Pharmacological
Thrombolysis (break down clots)
Aspirin
Modifiable risk factors
Physiotherapy

29
Q

Drugs and receptors

A

Effect after synaptic function

Agonist - increase NT
Antagonist - decrease NT

direct= attaches to NT binding site
indirect = drug binds to alternative binding site
Non-competitive binding = does not compete with NT

30
Q

Pharmacological treatments

A

Neuroprotection - aims to protect neurones from injury (limited by time window and effectiveness)

NMDA receptor antagonists - obvious choice for treating stroke

31
Q

NMDA receptor antagonists

A
  • Proved to be the most successful compounds ever generated to protect against cell death in vitro and in vivo (models)
  • Various compounds developed

ALL clinical trials have failed, why?
Lack of efficacy
Toxic side effects

32
Q

Aspirin

A
  • Antiplatelet agents (and anticoagulant)
  • Prevention of recurring strokes
  • Reduction of severity of stroke
    Inhibit production of thromboxane (decrease natural levels of blood clotting)
33
Q

Physiotherapy

A
  • Weakness/paralysis
  • Improve motility/avoid injury
  • Re-gain everyday activities
  • Promote Independent living
  • Exercise, manipulation, massage, skills training, electrical treatment

B and Neuro (17 decks)

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