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C&M Neuroanatomy > Week 9: Parkinson's disease > Flashcards

Week 9: Parkinson's disease Flashcards

1
Q

What are the top 2 most common neurodegenerative conditions?

A
  1. Alzheimer’s

2. Parkinson’s

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2
Q

What is parkinsonism?

A 
A clinical syndrome comprising of:
-bradykinesia
and at least one of:
-tremor
-rigidity
-postural instability
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3
Q

What is the most common cause of parkinsonism?

A

parkinson’s disease

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4
Q

What are the specific clinical symptoms of PD?

A
  • asymmetry of parkinsonism symptoms at onset

- sustained response to levodopa medication

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5
Q

What are the 4 causes of parkinsonism?

A
  1. Neurodegenerative conditions
  2. Drug-induced
    - dopamine antagonists (anti-psychotics)
  3. Vascular
  4. Metabolic
    - Wilson’s disease
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6
Q

Which 3 neurodegenerative conditions make up the umbrella term ‘parkinson’s plus’?

A
  1. Dementia with lewy bodies
  2. Progressive supranuclear palsy
  3. Multiple system atrophy
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7
Q

What are the risk factors for idiopathic/sporadic PD?

A
  • advancing age
  • M>F ratio 3:2
  • caucasians > asians and africans
  • rural living and farmers -pesticides
  • family history
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8
Q

Which lifestyle factors are said to decrease the risk of PD?

A
  • tobacco
  • coffee
  • NSAID use
  • alcohol consumption
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9
Q

Explain the two pathological hallmarks of PD

A
  1. Early degeneration and death of dopaminergic neurones within the substantia nigra pars compacta of the basal ganglia (lack of dopamine)
  2. Abnormal a-syn-lewy body protein and lewy neurite
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10
Q

Explain symptoms that might be present in the prodrome phase of PD

A

(before diagnosis)

  • constipation
  • RBD (REM sleep behaviour disorder)
  • EDS (excessive daytime sleepiness)
  • hyposmia - reduced sence of smell
  • depression
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11
Q

What are the symptoms after diagnosis in order of progression?

A
  • pain
  • fatigue
  • tremor
  • rigidity
  • anosmia
  • bradykinesia
  • urinary symptoms
  • dementia
  • dyskinesia
  • dysphagia
  • postural instability
  • freezing of gait
  • psychosis
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12
Q

How do we diagnose PD?

A

Diagnosis is made based on movement/motor symptoms and clinical examination:

  • asymmetric signs
  • bradykinesia plus at least one of: tremor, rigidity, postural instability
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13
Q

What is bradykinesia?

A
  • slow and small movements with less rhythm
  • slowed gait with shuffling steps
  • reduced facial expression (hypomimia) and blinking
  • reduced gesticulation
  • small hand writing (micrographia)
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14
Q

What is freezing of gait?

A
  • difficulty initiating movement
  • slowed pace
  • small steps
  • sttooped, flexed posture
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15
Q

What are the features of the tremor in PD?

A
  • in 70% of cases
  • usually begins in one hand, then spreads bilaterally
  • 4-7 Hz
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16
Q

How could we diagnose PD through imaging?

A
  • CT, MRIs in PD are usually normal

- DaTscan - nuclear medicine sam - abnormal in PD but exposes patients to radiation and isn’t specific for PD

17
Q

What is the gold standard medication for PD?

A

Levodopa (L-dopa): dopamine replacement –> increases dopaminergic stimulation of basal ganglia neurones

18
Q

What drug is given to prevent levodopa being broken down before reaching the brain?

A

dopa decarboxylase inhibitor

19
Q

What are the adverse effects of too much dopaminergic stimulation?

A
  • dyskinesia
  • dystonia/chorea
  • confusion
  • hallucinations
  • impulse control disorders
20
Q

What happens to the therapeutic window as PD progresses in a patient?

A
  • therapeutic window narrows

- so patient will have more ‘off’ time when the medication isn’t working or is working too much (hyperkinetic)

21
Q

What are 3 key features of neurodegenerative disorders?

A
  • loss of neurones
  • progressive
  • irreversible
22
Q

How is PD an ‘akinetic-rigid’ syndrome?

A

loss of voluntary movement, increased muscle tone

23
Q

What is the most common cause of death associated to PD?

A

Bronchopneumonia

24
Q

Which pathway is lost in PD?

A

Nigro-striatal inhibitory/excitatory pathway

25
Q

Which drugs decrease dopamine breakdown?

A

MAO and COMT inhibitors

26
Q

Why do we give L-DOPA as a combination therapy?

A
  • usually, only 1% of L-DOPA would reach the brain, the rest would be metabolised in the intestines
  • we overcome this by giving l-dopa with carbidopa which prevents breakdown of L-DOPA
27
Q

What are some adverse effects of L-DOPA?

A
  • ‘on-off’ effects –> worsening of PD symptoms
  • nausea, vomiting, anorexia
  • dyskinesias
  • tachycardia
  • hypotension
  • insomnia, confusion
28
Q

What does selegiline do?

A

prevents breakdown of dopamine

29
Q

How is Huntington’s the mirror opposite of PD?

A
  • it is a disorder of excessive and continual movement
  • main symptoms are chorea and dementia
  • starts at 30-50 typically
  • juvenile onset more severe
30
Q

what are the symptoms of Huntington’s?

A
  • irritability
  • moodiness
  • antisocial behaviour
  • fidgeting
  • restlessness
  • dementia
  • gross choreiform movements
31
Q

Why does a huntington patient find it difficult to stop movement?

A
  • we’re loosing the inhibitory outputs from the striatum that project to the thalamus and back to the substantia nigra
  • mutation in protein called huntingtin
  • selective cell loss in cerebral cortex and corpus striatum
32
Q

How is Huntington’s inherited and where is the gene defect?

A
  • autosomal dominant
  • gene defect on short arm of chromosome 4
  • gives rise to an expanded and repeated CAG

C&M Neuroanatomy (44 decks)

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