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Applied Health Science > Common Neurological Conditions > Flashcards

Common Neurological Conditions Flashcards

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1
Q

What is alzeimers disease?

A

Cognitive impairment leading to dementia
Most common cause of dementia
Distinct pathological signature emerging
Huge social and economic burden
- Mainly happening after 65 years old
- Early onset – 5% - under 65 years old – some genetic linking

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2
Q

State some deficients of alzeimers disease

A

Sensation – speed processing – perception – motor skills – executive functioning – language – memory

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3
Q

What are the key anatomical features of Alzheimers disease?

A

Cortical atrophy - tissue loss

  1. Loss of parenchyma
  2. Hydrocephalus ex vacuo – tissue loss – increased size of ventricles
  3. Narrow gyri
  4. Widened Sulci
  5. Atrophy of parahippocampal cortex – base of brain – memory forming loss
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4
Q

State the two sections of the pathological signature of Alzheimers disease

A
  1. Senile plaques – AKA neurotic plaques/ amyloid plaques
  2. Neurofibrillary tangles
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5
Q

What are two other names for amyloid plaques?

A

Senile or neurotic plaques

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6
Q

What are amyloid plaques?

A

1.Extracellular deposits of beta amyloid (inflammatory cells and deposits build up)
2. Recruitment of activated astrocytes (removed inflammatory build up) and microglia (local inflammatory response)
3. Dystrophic neuritis locally (spouting/ expansion of proteins/ other cells)
(Number and distribution not scientifically correlated)

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7
Q

How is beta amyloid formed?

A
  1. Amyloid precursor protein APP
  2. Alpha and gamma secretes enzymes
  3. Other peptides losses
  4. Beta amyloid formed
  5. Secreted from neurone into tissue around nerve cells - stack up of molecules (oligomer then protofibril then fibril) – if this is miss-folded which enhances accumulation of protein around the cell
  6. Amyloid plaque develops from this accumulation
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8
Q

Whats the hypothesis for how amyloid leads to Alzheimers?

A

Amyloid cascade hypothesis

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9
Q

What is the amyloid cascade hypothesis?

A
  1. Amyloid accumulation may be the initial step in alzheimer’s dementia pathogenesis
  2. Leading to deposition of Tau protein (neurofibrillary tangles)
  3. Taupathy is linked to neuronal decline and synaptic loss
  4. These in turn result in classical cognitive decline (tissue loss)
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10
Q

How has Tau protein production effect alheimers?

A

Important link in causing the loss of neurons and synapses.

with link to inflammatory mechanisms

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11
Q

What are Tau proteins?

A
  • Usually very soluble protein that encoded by MAPT gene
  • Stabilising the cytoskeleton of neuron networks in axons (inside the neuron cells)
  • Important for axonal transport – movement of transport vesicles – forming deposits
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12
Q

What are MAPT gene?

A
  • Microtubule associated protein Tau
  • Stabilising microtubule (cytoskeleton) network in axons
  • Abundant in neurons of CNS
  • Microtubules important for axonal transport – movement of transport vesicles and important molecules
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13
Q

What are neurofibillary tangles?

A
  • Formed from Tau protein
  • Tau becomes insoluble when its highly phosphorylated
  • Hyperphosphorylaed Tau – insoluble
  • Accumulated in cytoplasm
  • Fine filaments observable
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14
Q

What is the Tau hypothesis of Alzheimers disease?

A

Correlation for profession of disease and increase in amyloid plaque

  • Tau pathology
  • Primary driver of neurodegeneration
  • Insoluble and goes inside the neuron to phosphorylate

Distribution of tangles correlates with clinical dementia rating
Spread of Tau pathology correlated with cognitive decline and neuron loss
Pathology spreads from neuron to neuron

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15
Q

How are Tau proteins spread to cause degeneration in neurons?

A
  1. NF tangle inside neurone
  2. Goes towards synapse by diffusion
  3. Filament fragments transferred trasnsynaptically (across the synaptic cleft)
  4. Second neuron seeded and new tangles develop
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16
Q

What does Tauopathy do to neurons?

A

1.Disruption to functioning of cytoskeleton
2. Disruption to receptor protein trafficking inside cell
3. Disruption to synapse function and formation

IN the end these issues lead to neuronal death

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17
Q

Whats the overall effect of tauopathy?

A

IN the end these issues lead to neuronal death

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18
Q

What is the role of inflammtion in Alzheimers dementia?

A

Amyloid deposition turns microglia cells to activated microglia cells (cells in brain regulate brain development, maintain neuronal pathways and injury repaire)

  1. Activated microglia/astrocytes prominent feature in AD pathology
  2. Genetic linkage with regulators of microglia function

Correlation between activation of microglia and AD pathology

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19
Q

As symptomatic Alzheimers disease develops what does pathology show?

A
  • Reduction in synaptic and neuronal function and density
  • Increase in amyloid beta deposition, microglia and astrocytes activation, Tau pathology
20
Q

What does activated microglia do?

A
  • Inhibits seeding of amyloid beta and remove amyloid beta by endocytosis
  • Inhibits seeding of Tau

But Amyloid beta endocytosis activates release of damaging inflammatory mediators

21
Q

How is the ageing brain effected by Alzheimers disease?

A

By 20 years old neuronal deficit has begun.

(linked to deposition of amyloid plaque) and neuromelanin pigments of neural tissue as we age

22
Q

How is age related to issues with the brain?

A
  • Hippocampus loses mass - Short term memory problems
  • Motor cortex increased neuronal atrophy – gate and movement deficit
  • Autonomic centres respond less rapidly – postural hypertension – dizziness as sitting or standing
  • Reducing integrity of blood brain barrier – pathogens and harmful substances ins to brain tissue (inflammatory)
  • Neurotransmitter production reduced
  • Mitochondrial dysregulation – reduction of production of brain cells
23
Q

Whats the gross anatomy of meninges?

A
  1. Dura mater (thick) - periostea’s and meningeal layers
  2. Arachnoid mater – sub arachnoid space containing cerebrospinal fluid
  3. Pia mater – nutritive layer hugging surface of the brain
24
Q

Why associated brain and microbiome?

A

Brain inclosed, edged space (little room for expansion)
Close to areas containing wet mucosa (associated with complex microbiome)
Microbiome may contain – commensal, parasitic and/or pathogenic organisms

25
Q

Why can the blood-brain barrier be seen as good?

A

Helps to isolate the brain from circulatory system
Protect areas against
- Toxins
- Pathogens
- Blood components

26
Q

What is the blood-brain barrier absent in?

A

1.Choroid plexus – where cerebrospinal fluid is produced
2. Posterior pituitary and neurohypophysis

27
Q

Explain the Epidemiology of bacterial meningitis

A
  • 50% mortality if untreated
  • All age groups effects due to infection and inflammation
  • Much fewer in more developed countries
    Different ages efffected by different strains

Emerging antibiotic resistance

28
Q

What is the pathophysiology of bacterial meningitis?

A
  1. Inflammation of meninges
  2. Particularly arachnoid mater and pia mater
  3. Bacteria invade subarachnoid space
  4. Spreading to ventricles (ventriculitis)
  5. Infection spreads to brain parenchyma – spinal cord
  6. Neuronal damage – particularly hippocampus
    Highly activated leukocytes in cerebrospinal fluid
29
Q

How does bacteria gain access to cerebrospinal fluid?

A

1.Local defects
2.Sites of infection – endothelial damage
3. Choroid plexus – areas where neurohormones are released.

30
Q

What does bacterial affect in bacterial meningitis?

A

Bacteria -> bacterial toxins or activate leukocytes (both inflammatory medications and untoimmune damage ) -> deems, intracranial pressure, neuronal damage

31
Q

What are the causes of bacterial meningitis?

A
  1. Soluble bacterial toxins
  2. Toxins inflammatory mediators
  3. Trigger dangerous inflammatory response
  4. Edema in tissues
  5. Pus in subarachnoid space
  6. Spreading over cerebrum, cerebellum, spinal cord
  7. Pus that block CSF flow and reabsorption
    Leading to elevated intracranial pressure
32
Q

What are the secondary effects of inflammation?

A

ICP and edema can have profound effects

33
Q

Wat is a primary brain injury?

A

Initial insult – the processes of physical displacement
Ultimate driver of secondary brain injury

Eg.
Shearing and tearing of blood vessels, neurons, glia and secondary injury
Mechanical tissue deformation resulting in necrotic cell death

34
Q

What is a secondary brain injury?

A

Gradually developing post trauma pathology
- Decreased CBF (ischaemic) and Increased ICP – haemorrhage or edema

35
Q

what is Intra-cranial pressure
(Adult)?

A

Cranial volume is fixed
Brain tissue, blood and cerebrospinal fluid ~1700ml

Tissue + blood + CSF = total volume
An increase in one leads to a matching decrease in either one or both of the remain two as total volume is fixed.

36
Q

What is the monro-kellie doctrine?

A

Relationship between the contents of the cranium and intracranial pressure
Normal IC pressure is 7-15mmHg

increase in one pressure means decrease in another as same pressure

37
Q

Explain the Pathology of intra-cranial pressure
CHanges in tissue volume

A

Meningitis
Brain tumour
Inglammation and oedema (trauma and infection)
Haemorrhage

38
Q

Whats the Pathology of intracranial pressure
Changes to CSF volume

A

Choroid plexus tumour
Blockage retarding CSF flow
Reduced drainage into venous sinus

39
Q

Whats the Pathology of intracranial pressure
Changes to blood volume

A

Hyper apnea – local vasodilation
Heart failure 0 increased venous pressure

40
Q

Whats the Systemic effects of extreme intracranial pressure?

A
  1. Rising blood pressure
  2. Slowing pulse
  3. Periodic of slowing respiration
41
Q

Whats the effects of Rising blood pressure in response to extreme intracranial pressure ?

A

-Ischaemic response in hypothalamus drives sympathetic activation
- peripheral vasocoscruction
- increased cardiac output via tachycardia reflex – activation of cardiac beta 1 adrennergic receptors
- increased systemic blood pressure

42
Q

Whats the effect of Slowing pulse in response to extreme intracranial pressure?

A

Increase blood pressure activates peripheral baroreceptors
- Sensory feedback to brain stem and parasympathetic compensation
- Leads to overall bradycardia (activation of cardiac M2 muscarinic AChRs)

43
Q

Whats the effect of Periodic or slowing respiration in response to extreme intracranial pressure ?

A

Ischaemic response drives hypoventilation/ apnoea
- Iaschemic damage and physical pressure on brain stem
- Depolarisation of respiratory pacemaker cells
- Dysregulation of breathing pattern

44
Q

Whats the cushing triad?

Indicative or high ICP?

A
  1. Rising blood pressure
  2. Slowing pulse
    Periodic or slowing respiration
45
Q

How does compensation effect intra-cranial pressure?

A

Increased venous drainage
And/or
Increased CSF drainage

ICP above 20mmHg

46
Q

What are the 4 types of herniation?

A
  • In transcalvarial – herniation out fracture or surgical site/hole
  • Cingulate (subfalcine) – frontal lobe
  • Uncal – move intracranial compartment to another c
  • Tonsillar herniation – push down on brain stem – downward cerebeller – mortal

Applied Health Science (11 decks)

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