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Neuropsychiatric Disorders > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What is the second most common neurodegenerative disease?

A

Parkinson’s disease

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2
Q

What is the mean age of PD onset?

A

65

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3
Q

What are the most common risk factors for PD?

A

▪️ Male (1.5x)
▪️ Family history
▪️ Head injury
▪️ Pesticide exposure

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4
Q

What are the key motor symptoms of PD?

A

▪️ Tremor at rest
▪️ Rigidity (stiffness)
▪️ Bradykinesia (slowness)
▪️ Hypokinesia (poverty of movement)

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5
Q

What is the main motor indicator of early PD?

A

Unilateral signs and symptoms

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6
Q

How do the motor symptoms of PD changes as the disease progresses?

A

Become bilateral

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7
Q

What is the Hoehn and Yahr scale?

A

A measure of functional disability in PD

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8
Q

What are stages 1 and 2 on the Hoehn and Yahr scale?

A

Mild disability:

  1. Unilateral involvement with minimal or no functional disability
  2. Bilateral or midline involvement without impairment of balance
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9
Q

What is stage 3 on the Hoehn and Yahr scale?

A

Moderate disability:

▪️ Bilateral disease
▪️ Mild to moderate disability but physically independent
▪️ Impaired postural reflexes

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10
Q

What are stages 4 and 5 on the Hoehn and Yahr scale?

A

Severe disability:

  1. Severely disabling disease, still able to walk or stand unassisted
  2. Confinement to bed or wheelchair unless aided
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11
Q

What are some of the main non-motor symptoms of PD?

A

▪️ Neuropsychiatric/cognitive disorder
▪️ Sensory disorders
▪️ Medication-induced effects (e.g., ICD)
▪️ Urinary disorders and autonomic dysfunction
▪️ Fatigue and sexual dysfunction
▪️ Sleep disorder
▪️ Gastrointestinal disorders

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12
Q

What are the most common neuropsychiatric and cognitive symptoms of PD?

A

▪️ Psychosis (possibly drug-induced)
▪️ Depression
▪️ Anxiety
▪️ Apathy
▪️ Dementia
▪️ Hallucinations (particularly small children and animals)

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13
Q

What is DDS/ICD?

A

Dopamine Dysregulation Syndrome / Impulse Control Disorder

▪️ Behavioural problems resulting from prolonged use of dopaminergic medication such as L-DOPA
▪️ Characterised by increased gambling behaviours, hypersexuality, aggression, spending, binge eating etc

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14
Q

What symptoms in PD have the strongest correlation with quality of life?

A

Non-motor symptoms

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15
Q

What percentage of dopaminergic neurons are lost before motor symptoms become apparent?

A

50-70%

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16
Q

When is the prodromal stage of PD and what are the main symptoms?

A

Up to 20 years before motor symptoms

▪️ Hyposmia
▪️ Sleep disruption (e.g. RBD, loss of REM atonia)
▪️ Depression
▪️ Constipation

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17
Q

How long is the early motor stage of PD and what symptoms may become apparent?

A

3-6 years

▪️ Fatigue
▪️ Pain (subtle motor deficit?)
▪️ Diplopia (double vision)

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18
Q

How long is the mid stage of PD and what symptoms may become apparent?

A

4-12 years

▪️ Anxiety
▪️ Hypophonia (reduced speech intensity)
▪️ Dysphagia
▪️ Sleep disturbance (e.g., fragmentation)

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19
Q

How long is the late stage of PD and what symptoms may become apparent?

A

8 years

▪️ Dementia
▪️ Cognitive dysfunction
▪️ Hallucinations
▪️ Incontinence
▪️ Sexual dysfunction
▪️ Orthostatic hypotension (sudden BP drop when stand up)

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20
Q

What is the main pathological marker of PD?

A

▪️ Loss of dopaminergic neurons in the substantia nigra
▪️ Presence of Lewy bodies (abnormal accumulation of alpha-synuclein)

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21
Q

What are constant levels of dopamine necessary for?

A

▪️ Regulation of cortical excitation of striatal neurons
▪️ Stabilisation of the firing rate and excitability of striatal neurons
▪️ Modulations of plasticity of striatal neurons (LTP)

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22
Q

According to the Braak staging, where does Lewy body pathology start?

A

Olfactory bulb (explains prodromal hyposmia)

23
Q

Where does the pathology spread to in the middle Braak stages?

A

▪️ Midbrain - substantia nigra (explaining onset of motor symptoms)
▪️ Neocortex

24
Q

Where does PD pathology spread to in the late Braak stages?

A

Through the cortex (explaining cognitive dysfunction and dementia)

25
Q

According to newer models of PD, what are the two subtypes?

A

▪️ Body-first PD
▪️ Brain-first PD

26
Q

How is pathology proposed to spread in the body-first subtype of PD?

A
  1. Begins in gastrointestinal tract (explains constipation)
  2. Cardiovascular system and dorsal motor nucleus
  3. Locus coeruleus
  4. Substantia nigra
  5. Cortex
27
Q

How does the brain-first PD subtype differ from the body-first subtype?

A

▪️ Begins in substantia nigra
▪️ Absence of classic non-motor prodromal phase

28
Q

What other neurotransmitters may be involved in PD, contributing to the clinical heterogeneity?

A

▪️ Serotonin
▪️ Noradrenaline
▪️ Acetylcholine

29
Q

What is required for the diagnosis of PD?

A

Motor symptoms - usually the triad of tremor, bradykinesia, and rigidity

30
Q

What type of scan can be used to support PD diagnosis?

A

DaTSCAN

31
Q

How does DaTSCAN work?

A

▪️ Radioactive nucleotide injected
▪️ Binds to dopamine transporters
▪️ Visualise using SPECT
▪️ Decreased binding in PD due to loss of dopaminergic neurons

32
Q

What are the three things you can look for with a DaTSCAN?

A

▪️ Decreased binding indicating decreased dopamine uptake
▪️ Symmetry of decrease
▪️ Gradient - usually putamen lost first, followed by caudate

33
Q

What percentage of PD patients have olfactory dysfunction?

A

70-100%

Typically underreported
Usually prodromal hyposmia but in same cases its late onset or complete anosmia

34
Q

What can you use to test olfactory function?

A

UPSIT

(University of Pennsylvania Smell Identification Test)

35
Q

What PD pathology likely underpins the increased prevalence of prodromal RBD?

A

Alpha-synuclein

36
Q

What percentage of PD cases can be attributable to genetic mutations?

A

5-10%

37
Q

What is the status of genetic testing in PD?

A

▪️ Not routine and costly
▪️ Presently unhelpful - no treatments that can be offered based on findings
▪️ May be inconclusive
▪️ Currently research based

38
Q

What other degenerative disease may present with Parkinsonism?

A

▪️ Multiple System Atrophy
▪️ Progressive Supranuclear Palsy

39
Q

What differential diagnoses should be consider when assessing for PD?

A

▪️ Other causes of parkinsonism (e.g., MSA, PSP, drug-induced, vascular, infections)
▪️ Tremor disorders (e.g., essential tremor, dystonic tremor)

40
Q

If someone presents with only a tremor, what should you consider in diagnosis?

A

▪️ Essential tremor
▪️ Dystonic tremor

41
Q

How might you distinguish essential tremor from PD?

A

▪️ Tremor not present at rest, only when performing action
▪️ Very symmetrical

(BUT can sometimes develop PD later so should observe patients carefully!)

42
Q

What are the three main approaches to pharmacological treatment of PD?

A

▪️ Increase levodopa levels
▪️ Inhibit MAO and COMT enzymes to prevent dopamine breakdown
▪️ Dopamine receptor agonists

43
Q

What are the three main options for the pharmacological treatment of PD?

A

▪️ Levodopa
▪️ Monoamine oxidase B inhibitor
▪️ Dopamine agonist

44
Q

How do you choose which medication to use?

A

Personal preference based on side effects, comorbidities etc

(e.g., younger individual may prefer more potent treatment to function better)

45
Q

What happens with levodopa therapy in the early stages of disease?

A

▪️ Smooth, long duration of benefit
▪️ Low incidence of dyskinesias (uncontrolled, erratic movements)

46
Q

What happens with levodopa therapy in the mid-stage of disease?

A

▪️ Rapid onset of benefit due to more diminished dopamine stores
▪️ Diminished duration of benefit
▪️ Increased incidence of dyskinesias
▪️ Fall after peak dyskinesia

47
Q

What happens with levodopa therapy in the advanced stage of disease?

A

▪️ Clinical response mirror levodopa plasma
▪️ Much shorter duration of benefit
▪️ ‘On’ time is associated with dyskinesias
▪️ Steep drop back to ‘off’ time

48
Q

What motor complications are often seen in the later stages of disease?

A

Dopamine-induced motor fluctuations

“On/off” phenomena with dyskinesia (unstable PD)

49
Q

What are the two key factors involved in the development of motor fluctuations?

A

▪️ Progressive degeneration - loss of ability to store dopamine and release it slowly
▪️ Pulsatile stimulation - typically take tablets three times daily, little we can do in between doses

50
Q

What can we use to prevent motor fluctuations and development of dyskinesias?

A

Non-oral therapies and continuous drug delivery (CDD) (e.g., infusions)

51
Q

What is the first-line option for continuous dopamine delivery?

A

Transdermal rotigotine

(Patch that releases dopamine continuously over 24 hours)

52
Q

What more invasive options could be considered for CDD?

A

▪️ Subcutaneous apomorphine infusion (dopamine agonist in an insulin-like pump)
▪️ Intra-jejunal levodopa infusion (PEG, required surgery, patient can control dose)

53
Q

Where are electrodes typically placed for the use of DBS in PD?

A

Subthalamic nucleus

Neuropsychiatric Disorders (30 decks)

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