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Neurology > Parkinson's disease > Flashcards

Parkinson's disease Flashcards

1
Q

What are the two components of the brain that feed into the upper motor neuron system?

A

Basal ganglia

Cerebellum

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2
Q

What is Parksinson’s a disease of?

A

The basal ganglia

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3
Q

Name the components of the basal ganglia system.

A 
Corpus striatum
- Caudate nucleus 
- Putamen
Globus pallidus
Substantia nigra
Thalamus
Subthalamic nuclei
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4
Q

Name the loops of the basal ganglia and their function.

A

Motor - movement
Oculomotor - eye movement control
Lateral orbito-frontal - social behaviour
Dorsolateral prefrontal loop - executive functions and working memory

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5
Q

What is the input and output of posture and voluntary movement control in the basal ganglia?

A

Input: cortex
Output: cortex and brainstem

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6
Q

Describe the epidemiology of Parkinson’s disease.

A 
180 per 100,000
3men:2women 
Prevalence increases >60 years
Mean duration from diagnosis to death is 15 years
Sporadic disorder
Monogenic causes (6% of cases)
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7
Q

What are the most common monogenic causes of Parkinson’s?

A

Mutation in

  • LRRK2 protein
  • Parkin protein
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8
Q

Describe the pathology of Parkinson’s disease.

A

Degeneration of dopaminergic neurons within the substantia nigra (dopamine being the main neurotransmitter in substantia nigra)
- dopamine concentrations decrease
- lack of dopamine in the basal ganglia
- biggest loss within the nigrostrial pathway
The surviving neurons accumulate an abnormal type of the protein alpha-synuclein within Lewy bodies
- cytoplasmic inclusion bodies

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9
Q

How do people have Parkinson’s disease for years before symptoms?

A

The basal ganglia can lose 50-60% of it’s dopamine concentrations before it stops compensating
- then motor symptoms appear

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10
Q

Name some possible mechanisms for Lewy body formation.

A 
Oxidative stress
Mitochondrial 
Excitotoxicity 
Protein aggregation 
Interface with DNA transcription 
Nitric oxide 
Inflammation 
Apoptosis
Trophin deficiency 
Infection
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11
Q

Describe the Lewy body staging of Parkinon’s disease.

A

Stage 1-2
- Lewy bodies first appear in the pons/medulla and olfactory nucleus
- presymptomatic or pre-motor stage (e.g. loss of smell)
Stage 3-4
- Lewy bodies next appear in the midbrain (substantia nigra pars compacta)
- Parkinsonism become evident after extensive nigral damage
Stages 5-6
- Lewy bodies finally involve the neocortex
- development of PD dementia

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12
Q

What are the clinical features of Parkinson’s?

A 
4 main motor symptoms
- bradykinesia
and at least one of
- muscular rigidity
- 4-6 Hz rest tremor (quite a slow, asymmetric tremor)
- postural instability
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13
Q

What is bradykinesia?

A

Slowness in initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions (movement becomes slower and smaller)

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14
Q

Name the non-motor symptoms of Parkinson’s disease.

A 
Neuropsychiatric
- dementia
- depression
- anxiety
Autonomic 
- constipation 
- urinary urgency/nocturia 
- erectile dysfunction 
- excessive salivation 
- postural hypotension
Sleep
- REM sleep behaviour disorder
- restless legs syndrome 
- daytime somnolence 
Other
- reduced olfactory function
- fatigue 
- pain and sensory sensation
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15
Q

Name some differential diagnosis of Parkinson’s disease.

A

Benign tremor disorder (e.g. essential tremor)
Dementia with Lewy bodies
Vascular Parkinsonism
Parkinson plus disorders (e.g. progressive supranuclear palsy, multiple system atrophy)
Drug-induced parkinsonism/tremor
- caused by drugs that block dopamine

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16
Q

If you suspect someone has Parkinson’s disease, what investigations would you perform?

A

Bloods
- if tremor present; thyroid function and copper tests (e.g. Wilson’s disease)
Structural imaging
- CT/MRI brain normal in Parkinson’s disease
- abnormal in vascular parkinsonism and Parkinson plus disorders
Functional imaging
- imaging of presynaptic dopaminergic function using DAT SPECT is abnormal in degenerative Parkinsonism

17
Q

In a normal DATSCAN, where is the uptake highest?

A

In the middle slices of the striatum

18
Q

What happens in a FC-CIT SPEC in Parkinson’s disease?

A

As dopamine neurons are lost, they can’t take up to DAT SPECT, and the middle part of the striatum glows less
- asymmetric loss

19
Q

What is the aim of pharmacological treatment of Parkinson’s?

A

To restore dopamine levels

20
Q

What is the clinical aim of treating Parkinson’s?

A

Improve motor symptoms and quality of life

21
Q

Name the drug classes used to treat Parkinson’s.

A

L-DOPA
Dopamine agonists
MAO-B inhibitors
COMT-inhibitors

22
Q

Describe the mechanism of action of L-DOPA.

A

Absorbed in the stomach and taken in through the BBB

It is taken up by dopaminergic neurons, where it is decarboxylated to dopamine within the presynaptic terminals

23
Q

What are the two most common preparations of L-DOPA?

A

L-DOPA and carbidopa = Sinemet
L-DOPA and benserazide = Madopar
It is prescribed with a drug that prevents L-DOPA breakdown before it reaches the BBB

24
Q

What are the adverse effects of L-DOPA?

A

Peripheral
- nausea, vomiting and postural hypotension
Central
- confusion and hallucinations
Long term (5 years) - 50% of patients
- fluctuation in motor response
- dyskinesia (chorieform movements at peak dose)

25
Q

Name some examples of dopamine agonists.

A

Ropinirole
Pramipexole
Rotigotine
Apomorphine

26
Q

What is the mechanism of action of dopamine agonists?

A

Act directly on post-synaptic striatal dopamine receptors (D2 subtype)
- increase sensitivity to dopamine in the brain

27
Q

When are dopamine agonists used?

A

Either in early disease, or in combination with L-DOPA

28
Q

What are the pros and cons of dopamine agonists over L-DOPA?

A 
Pros
- longer half life
- fewer motor complications
Cons
- not as effective
29
Q

What are the side effects of dopamine agonist treatment?

A

Dopaminergic side effects
Somnolence
Impulse control disorders (hypersexuality, gambling)
Nightmares

30
Q

Name the two type of enzyme inhibitor drugs that are available.

A

MAO-B inhibitors
- selegiline, rasagiline
COMT inhibitors
- entacapone, tolcapone

31
Q

Describe the mechanism of action of MAO-B inhibitors.

A

Prevent dopamine breakdown by binding irreversibly to monoamine oxidase

32
Q

Describe the mechanism of action of COMT inhibitors.

A

Inhibit catechol-o-methyltransferase
- this results in a better half life and duration of action of L-DOPA
This means that is is co-prescribed with L-DOPA in later disease

33
Q

What are the side effects of COMT inhibitor use?

A 
Diarrhoea
Dopaminergic side effects
- nausea, vomiting
- headache
- constipation
- dizziness
- etc.
34
Q

Describe the complications found in advanced Parkinson’s disease.

A 
Motor complications
- on/off fluctuations
- L-DOPA induced dyskinesia 
Poor balance/falls
- worsening posture
Speech/swallowing problems
Dementia (at about 10 years)
35
Q

List the multi-disciplinary team involved in taking care of someone with Parkinson’s.

A 
GP
Neurologist 
Parkinson's disease nurse specialist 
Physiotherapist 
Speech and language therapist
Psychiatrist 
Psychologist 
Occupational therapist
Palliative care team
Neurosurgeon
36
Q

List some causes of parkinsonsim.

A 
Dementia with Lewy bodies
Progressive supranuclear palsy
Multiple system atrophy
Corticobasal degeneration 
Drug-induced (chronic use of dopamine antagonists)
Cerebrovascular disease
Toxins (e.g. carbon monoxide)
Post-infectious
37
Q

What are the main roles of the basal ganglia?

A

Maintaining posture

Initiating voluntary movement

38
Q

What is Parkinson’s disease?

A

Slowly progressive, asymmetric, neurodegenerative disorder that commonly affects the elderly

Neurology (13 decks)

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